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125 <!-- /burger-menu-wrap --> 126 127 <!-- header-menu-wrap --> 128 <div class="header-menu-wrap"> 129 <ul id="header-menu" class="header-menu"><li><a href="https://geckoconsortium.com/about-gecko/">About</a></li> 130<li><a href="https://geckoconsortium.com/"><img width="58" height="41" src="data:image/svg+xml,%3Csvg%20xmlns='http://www.w3.org/2000/svg'%20viewBox='0%200%2058%2041'%3E%3C/svg%3E" alt="Logo" class="logo-img" data-lazy-src="https://geckoconsortium.com/wp-content/themes/gecko/assets/images/logo.svg"><noscript><img width="58" height="41" src="https://geckoconsortium.com/wp-content/themes/gecko/assets/images/logo.svg" alt="Logo" class="logo-img"></noscript></a></li> 131<li><a href="https://geckoconsortium.com/#studies">Studies</a></li> 132</ul> 133 <div class="header-bar-bg"> 134 <svg class="header-svg" version="1.1" xmlns="http://www.w3.org/2000/svg" xmlns:xlink="http://www.w3.org/1999/xlink" x="0px" y="0px" 135 viewBox="0 0 415.4 150" style="enable-background:new 0 0 415.4 150;" xml:space="preserve"> 136<path fill="#FFFFFF" d="M298.7,0H0c9.5,0.7,18.9,2.8,27.9,6.2c4.9,1.9,12.1,5.4,23.9,16.7c17.8,17,15,22.3,26.9,28.2 137 c6.4,3.2,17.4,6.7,37,6.9v0h183c20.3-0.1,31.5-3.7,38-6.9c11.9-5.9,9.1-11.1,26.9-28.2c11.8-11.3,19-14.8,23.9-16.7 138 c9-3.4,18.3-5.5,27.9-6.2L298.7,0z"/> 139</svg> 140 <svg class="mobile-header-svg" xmlns="http://www.w3.org/2000/svg" xmlns:xlink="http://www.w3.org/1999/xlink" version="1.1" x="0px" y="0px" viewBox="0 0 287.5 150" style="enable-background:new 0 0 287.5 150;" xml:space="preserve"> 141 <path fill="#FFFFFF" class="st0" d="M206.7,0H0c6.8,0.8,13.3,2.9,19.3,6.2c3.4,1.9,8.4,5.4,16.6,16.7 c12.3,17,10.4,22.3,18.6,28.2c4.4,3.2,12,6.7,25.6,6.9v0h126.6c14-0.1,21.8-3.7,26.3-6.9c8.2-5.9,6.3-11.1,18.6-28.2 c8.2-11.3,13.2-14.8,16.6-16.7c6-3.3,12.5-5.4,19.3-6.2L206.7,0z"/> 142</svg> </div> 143 </div> 144 <!-- /header-menu-wrap --> 145 146 <!-- switcher-wrap --> 147 <div class="switcher-wrap"> 148 <div class="switcher-toggle" data-type="broad-type"> 149 <span class="broad-type switcher-btn active">Broad</span> 150 <span class="technical-type switcher-btn">Technical</span> 151 <div class="switcher-active-border"></div> 152 </div> 153 </div> 154 <!-- /switcher-wrap --> 155 156 </div> 157 </header> 158 <!-- /header --> 159 <main id="main" class="site-main"> 160 <section id="primary" class="content-area"> 161 162 163 <header class="entry-header" data-anim="fade-slide-up"> 164 <div class="container"> 165 <h1 class="entry-title">Publications</h1> </div> 166 </header> 167 168 <article class="entry-container post-485 page type-page status-publish hentry" data-anim="fade-slide-up"> 169 <div class="container"> 170 <div class="row"> 171 <div class="small-12 columns entry-content"> 172 173<h2 class="has-luminous-vivid-orange-color has-text-color" style="font-size:45px">2025</h2> 174 175 176 177<div class="wp-block-group alignwide"><div class="wp-block-group__inner-container"> 178<h3><strong>Effect of ultra-processed food consumption on male reproductive and metabolic health</strong></h3> 179 180 181 182<p>Preston JM, Iversen J, Hufnagel A, Hjort L, Taylor J, Sanchez C, George V, Hansen AN, Ãngquist L, Hermann S, Craig JM, Torekov S, Lindh C, Hougaard KS, Nóbrega MA, Simpson SJ, Barrès R. <strong>Cell Metab.</strong> 2025 Aug 22:S1550-4131(25)00360-2. doi: 10.1016/j.cmet.2025.08.004</p> 183 184 185 186<p class="has-vivid-cyan-blue-color has-text-color"><a href="https://www.cell.com/cell-metabolism/fulltext/S1550-4131(25)00360-2" target="_blank" rel="noreferrer noopener"><em>https://www.cell.com/cell-metabolism/fulltext/S1550-4131(25)00360-2</em></a></p> 187 188 189 190<p></p> 191 192 193 194<div class="wp-block-media-text alignwide is-stacked-on-mobile" style="grid-template-columns:30% auto"><figure class="wp-block-media-text__media"><img width="996" height="846" src="data:image/svg+xml,%3Csvg%20xmlns='http://www.w3.org/2000/svg'%20viewBox='0%200%20996%20846'%3E%3C/svg%3E" alt="" class="wp-image-582 size-full" data-lazy-srcset="https://geckoconsortium.com/wp-content/uploads/2025/09/fx1_lrg-1.jpg 996w, https://geckoconsortium.com/wp-content/uploads/2025/09/fx1_lrg-1-300x255.jpg 300w, https://geckoconsortium.com/wp-content/uploads/2025/09/fx1_lrg-1-768x652.jpg 768w" data-lazy-sizes="(max-width: 99
1946px) 100vw, 996px" data-lazy-src="https://geckoconsortium.com/wp-content/uploads/2025/09/fx1_lrg-1.jpg" /><noscript><img width="996" height="846" src="https://geckoconsortium.com/wp-content/uploads/2025/09/fx1_lrg-1.jpg" alt="" class="wp-image-582 size-full" srcset="https://geckoconsortium.com/wp-content/uploads/2025/09/fx1_lrg-1.jpg 996w, https://geckoconsortium.com/wp-content/uploads/2025/09/fx1_lrg-1-300x255.jpg 300w, https://geckoconsortium.com/wp-content/uploads/2025/09/fx1_lrg-1-768x652.jpg 768w" sizes="(max-width: 996px) 100vw, 996px" /></noscript></figure><div class="wp-block-media-text__content"> 195<p><strong>Highlights</strong></p> 196 197 198 199<ul><li>Compared with an unprocessed diet, UPF impaired cardiometabolic and reproductive health</li><li>The deleterious effects of a UPF diet were independent of total caloric intake</li><li>A UPF diet altered the balance of several hormones, including GDF-15 and FSH</li><li>A UPF diet was associated with higher serum concentration of the phthalate cxMINP</li></ul> 200</div></div> 201 202 203 204<div class="wp-block-columns"> 205<div class="wp-block-column"></div> 206 207 208 209<div class="wp-block-column"></div> 210</div> 211 212 213 214<p class="has-text-align-left has-normal-font-size">Consumption of ultra-processed food is associated with increased caloric intake and impaired health. Here, we conducted a nutrition trial (NCT05368194) with controlled, 2 à 2 crossover design and tested whether ultra-processed food impairs reproductive and metabolic fitness, with further aggravation by excess caloric intake. Comparing the response from an unprocessed to ultra-processed diet identified increased body weight and low-density lipoprotein (LDL):high-density lipoprotein (HDL) ratio, independent of caloric load. Several hormones involved in energy metabolism and spermatogenesis were affected, including decreased levels of growth/differentiation factor 15 and follicle-stimulating hormone. Sperm quality trended toward impairment, with a decrease in total motility. Differential accumulation of pollutants between the discordant diets were detected, such as decreased plasma lithium and a trend for increased levels of the phthalate mono(4-methyl-7-carboxyheptyl)phthalate (cxMINP) in serum, following the ultra-processed diet. Alteration in caloric load alone had distinct effects on the measured outcomes. This study provides evidence that consumption of ultra-processed food is detrimental for cardiometabolic and reproductive outcomes, regardless of excessive caloric intake.</p> 215</div></div> 216 217 218 219<hr class="wp-block-separator"/> 220 221 222 223<p></p> 224 225 226 227<h3><strong>Dietary macronutrients modulate the proteome of brown adipose tissue in males and their female offspring.</strong></h3> 228 229 230 231<p>Macartney EL, Senior AM, Crean AJ, Small L, Pulpitel TJ, Ruffino L, Nobrega MA, Barrès R, Simpson SJ. <strong><strong>Cell Reports</strong>. </strong>2025 Jul 24;44(8):116050</p> 232 233 234 235<div class="wp-block-columns"> 236<div class="wp-block-column"> 237<p>Dietary macronutrient composition in males influences brown adipose tissue (BAT) size and BAT size of daughters in C57BL/6J mice. However, the effects of macronutrients and paternal effects on BAT function have yet to be characterized. We investigated the effects of macronutrient composition on the BAT proteome in male mice and offspring. In fathers, >50% of the proteome was affected by macronutrients. We identified two clusters with inverse patterns that correlated with BAT mass. Notably, uncoupling protein 1 (UCP1) was reduced on low-fat diets that promoted increased BAT mass, while there were increased levels of proteins involved in protein turnover. The same diets also led to a reduction in proteins involved in purine biosynthesis (purines are often UCP1 inhibitors). We also found that paternal protein intake negatively affected basigin expression in daughters, a protein that regulates Ucp1 transcription. Our results show that macronutrients in males remodel the protein expression of BAT directly and in their daughters.</p> 238 239 240 241<p class="has-vivid-cyan-blue-color has-text-color"><a href="https://www.sciencedirect.com/science/article/pii/S2211124725008216?via%3Dihub" target="_blank" rel="noreferrer noopener"><em>https://www.sciencedirect.com/science/article/pii/S2211124725008216?via%3Dihub</em></a></p> 242</div> 243 244 245 246<div class="wp-block-column"> 247<figure class="wp-block-image size-large"><img width="996" height="996" src="data:image/svg+xml,%3Csvg%20xmlns='http://www.w3.org/2000/svg'%20viewBox='0%200%20996%20996'%3E%3C/svg%3E" alt="" class="wp-image-602" data-lazy-srcset="https://geckoconsortium.com/wp-content/uploads/2025/09/1-s2.0-S2211124725008216-fx1_lrg-1.jpg 996w, https://geckoconsortium.com/wp-content/uploads/2025/09/1-s2.0-S2211124725008216-fx1_lrg-1-300x300.jpg 300w, https://geckoconsortium.com/wp-content/uploads/2025/09/1-s2.0-S2211124725008216-fx1_lrg-1-150x150.jpg 150w, https://geckoconsortium.com/wp-content/uploads/2025/09/1-s2.0-S2211124725008216-fx1_lrg-1-768x768.jpg 768w" data-lazy-sizes="(max-width: 99
2476px) 100vw, 996px" data-lazy-src="https://geckoconsortium.com/wp-content/uploads/2025/09/1-s2.0-S2211124725008216-fx1_lrg-1.jpg" /><noscript><img width="996" height="996" src="https://geckoconsortium.com/wp-content/uploads/2025/09/1-s2.0-S2211124725008216-fx1_lrg-1.jpg" alt="" class="wp-image-602" srcset="https://geckoconsortium.com/wp-content/uploads/2025/09/1-s2.0-S2211124725008216-fx1_lrg-1.jpg 996w, https://geckoconsortium.com/wp-content/uploads/2025/09/1-s2.0-S2211124725008216-fx1_lrg-1-300x300.jpg 300w, https://geckoconsortium.com/wp-content/uploads/2025/09/1-s2.0-S2211124725008216-fx1_lrg-1-150x150.jpg 150w, https://geckoconsortium.com/wp-content/uploads/2025/09/1-s2.0-S2211124725008216-fx1_lrg-1-768x768.jpg 768w" sizes="(max-width: 996px) 100vw, 996px" /></noscript></figure> 248</div> 249</div> 250 251 252 253<hr class="wp-block-separator"/> 254 255 256 257<p class="has-medium-font-size"></p> 258 259 260 261<h3><strong>Healthy lifestyle before and during pregnancy to prevent childhood obesity â study protocol for a parallel group randomised trial – The PRE-STORK trial.</strong></h3> 262 263 264 265<p>Kornerup N, Danielsen JH, Sahl RE, Pico ML, Johansen MY, Knop FK, Bønnelykke K, Bergholt T, Kelstrup L, Foghsgaard S, Ghauri N, Grønlund E, Lund L, Vinter CA, Forman JL, Barrès R, Nielsen KK, Andersen A, Torekov SS, Grunnet LG and Vilsbøll T. <strong>BMJ Open</strong>. 2025 Jan 25;15(1):e087895.</p> 266 267 268 269<p class="has-vivid-cyan-blue-color has-text-color"><a href="https://bmjopen.bmj.com/content/15/1/e087895.long" target="_blank" rel="noreferrer noopener"><em>https://bmjopen.bmj.com/content/15/1/e087895.long</em></a></p> 270 271 272 273<p><strong>Introduction:</strong> The global prevalence of people living with overweight has tripled since 1975 and more than 40% of Danish women enter pregnancy being overweight. With the increasing rates of obesity observed in children, adolescents and adults, there is an urgent need for preventive measures. Risk factors for childhood obesity include maternal overweight or obesity before conception and excessive weight gain during pregnancy. Interventions aimed at modifying maternal lifestyle during pregnancy have demonstrated minimal positive or no impact on the health of the children. The ‘healthy lifestyle before and during pregnancy to prevent childhood obesity – the PRE-STORK trial’ aims to provide insights into the effect of a lifestyle intervention initiated before conception and continued during pregnancy in women with overweight or obesity, on neonatal adiposity in their children.</p> 274 275 276 277<p><strong>Methods and analysis:</strong> In this randomised, two-arm, parallel-group, controlled trial, we will include 360 women with overweight or obesity (aged 18-40; body mass index 25-44 kg/m<sup>2</sup>) and their partners. The women will be randomised to receive either standard of care or a lifestyle intervention focused on preconception body weight reduction, regular physical exercise, healthy diet and support from a mentor <em>before</em> and <em>during</em> pregnancy. The primary outcome is the difference in neonatal adiposity measured in their children at birth. Children conceived during the trial will constitute a birth cohort, monitoring the effects on their health until the age of 18 years.</p> 278 279 280 281<figure class="wp-block-image size-large"><img width="1024" height="435" src="data:image/svg+xml,%3Csvg%20xmlns='http://www.w3.org/2000/svg'%20viewBox='0%200%201024%20435'%3E%3C/svg%3E" alt="" class="wp-image-603" data-lazy-srcset="https://geckoconsortium.com/wp-content/uploads/2025/09/bmjopen-2025-January-15-1-F1.large_-1024x435.jpg 1024w, https://geckoconsortium.com/wp-content/uploads/2025/09/bmjopen-2025-January-15-1-F1.large_-300x128.jpg 300w, https://geckoconsortium.com/wp-content/uploads/2025/09/bmjopen-2025-January-15-1-F1.large_-768x326.jpg 768w, https://geckoconsortium.com/wp-content/uploads/2025/09/bmjopen-2025-January-15-1-F1.large_.jpg 1280w" data-lazy-sizes="(max-width: 1024px) 100vw, 1024px" data-lazy-src="https://geckoconsortium.com/wp-content/uploads/2025/09/bmjopen-2025-January-15-1-F1.large_-1024x435.jpg" /><noscript><img width="1024" height="435" src="https://geckoconsortium.com/wp-content/uploads/2025/09/bmjopen-2025-January-15-1-F1.large_-1024x435.jpg" alt="" class="wp-image-603" srcset="https://geckoconsortium.com/wp-content/uploads/2025/09/bmjopen-2025-January-15-1-F1.large_-1024x435.jpg 1024w, https://geckoconsortium.com/wp-content/uploads/2025/09/bmjopen-2025-January-15-1-F1.large_-300x128.jpg 300w, https://geckoconsortium.com/wp-content/uploads/2025/09/bmjopen-2025-January-15-1-F1.large_-768x326.jpg 768w, https://geckoconsortium.com/wp-content/uploads/2025/09/bmjopen-2025-January-15-1-F1.large_.jpg 1280w" sizes="(max-width: 1024px) 100vw, 1024px" /></noscript></figure> 282 283 284 285<p><strong>Ethics and dissemination:</strong>
285 The trial has been approved by the Regional Committee on Health Research Ethics in the Capital Region of Denmark (identification number H-22011403) and will be conducted in agreement with the Declaration of Helsinki. All results, whether positive, negative and inconclusive, will be disseminated at national or international scientific meetings and in peer-reviewed scientific journals.</p> 286 287 288 289<p><strong>Trial registration number:</strong> ClinicalTrials.gov: <a href="http://clinicaltrials.gov/show/NCT05578690">NCT05578690</a> (October 2022).</p> 290 291 292 293<hr class="wp-block-separator"/> 294 295 296 297<p></p> 298 299 300 301<h3><strong>A Guinea Pig Model of Pediatric Metabolic Dysfunction-Associated Steatohepatitis: Poor Vitamin C Status May Advance Disease</strong></h3> 302 303 304 305<p>Pedersen K, Poojari A, Colberg SF, Mechernsee SM, Iversen JF, Barrès R, Lykkesfeldt J, Tveden-Nyborg P. <strong>Nutrients</strong>.2025 Jan 15;17(2):291.</p> 306 307 308 309<p class="has-vivid-cyan-blue-color has-text-color"><a href="https://www.mdpi.com/2072-6643/17/2/291" target="_blank" rel="noreferrer noopener"><em>https://www.mdpi.com/2072-6643/17/2/291</em></a></p> 310 311 312 313<p><strong>Background/Objectives:</strong> Children and teenagers display a distinct metabolic dysfunction-associated steatohepatitis (MASH) phenotype, yet studies of childhood MASH are scarce and validated animal models lacking, limiting the development of treatments. Poor vitamin C (VitC) status may affect MASH progression and often co-occurs with high-fat diets and related metabolic imbalances. As a regulator of DNA methylation, poor VitC status may further contribute to MASH by regulating gene expression This study investigated guinea pigsâa species that, like humans, depends on vitC in the dietâas a model of pediatric MASH, examining the effects of poor VitC status on MASH hallmarks and global DNA methylation levels. <strong>Methods:</strong> Sixty-two juvenile guinea pigs were exposed to a high-fat diet for 16 weeks. <strong>Results:</strong> Juvenile guinea pigs exhibited hepatic histopathology representative of pediatric MASH, confirmed by portal inflammation and fibrosis. Consistent with pediatric MASH, juvenile guinea pigs displayed increased lobular and portal inflammation (p < 0.05 and p < 0.0001, respectively) but less steatosis (p < 0.001) compared to adults. Compared to the controls, the guinea pigs deprived in VitC showed lower body weight (p < 0.01), higher expression of hepatic inflammatory genes (p < 0.05), and a lower global hydroxymethylcytosine to methylcytosine ratio in the high-fat groups (p < 0.05). <strong>Conclusions:</strong> Our study validates guinea pigs as a model of pediatric MASH and suggests that VitC contributes to an altered gene expression signature through the regulation of DNA hydroxymethylation. We postulate that nutritional co-deficiencies in MASH, such as low VitC, may accelerate disease progression and deserve further attention.</p> 314 315 316 317<hr class="wp-block-separator"/> 318 319 320 321<p></p> 322 323 324 325<h3><strong>Exposure to childhood maltreatment is associated with specific epigenetic patterns in sperm.</strong></h3> 326 327 328 329<p>Tuulari, JJ, Bourgery, M, Iversen, J, Koefoed, TG, Ahonen, A, Ahmedani A, Kataja EL, Karlsson L, Barrès R*, Karlsson L*, Kotaja, N*. <strong>Molecular Psychiatry</strong>. 2025 Jun;30(6):2635-2644.</p> 330 331 332 333<div class="wp-block-columns"> 334<div class="wp-block-column" style="flex-basis:100%"> 335<p class="has-vivid-cyan-blue-color has-text-color"><a href="https://www.nature.com/articles/s41380-024-02872-3#Fig1" target="_blank" rel="noreferrer noopener"><em>https://www.nature.com/articles/s41380-024-02872-3#Fig1</em></a></p> 336 337 338 339<div class="wp-block-columns"> 340<div class="wp-block-column" style="flex-basis:100%"> 341<div class="wp-block-columns"> 342<div class="wp-block-column"> 343<div class="wp-block-columns"> 344<div class="wp-block-column"> 345<figure class="wp-block-image size-large"><img width="766" height="570" src="data:image/svg+xml,%3Csvg%20xmlns='http://www.w3.org/2000/svg'%20viewBox='0%200%20766%20570'%3E%3C/svg%3E" alt="" class="wp-image-607" data-lazy-srcset="https://geckoconsortium.com/wp-content/uploads/2025/09/Capture-decran-2025-09-17-120615-1.jpg 766w, https://geckoconsortium.com/wp-content/uploads/2025/09/Capture-decran-2025-09-17-120615-1-300x223.jpg 300w" data-lazy-sizes="(max-width: 766px) 100v
345w, 766px" data-lazy-src="https://geckoconsortium.com/wp-content/uploads/2025/09/Capture-decran-2025-09-17-120615-1.jpg" /><noscript><img width="766" height="570" src="https://geckoconsortium.com/wp-content/uploads/2025/09/Capture-decran-2025-09-17-120615-1.jpg" alt="" class="wp-image-607" srcset="https://geckoconsortium.com/wp-content/uploads/2025/09/Capture-decran-2025-09-17-120615-1.jpg 766w, https://geckoconsortium.com/wp-content/uploads/2025/09/Capture-decran-2025-09-17-120615-1-300x223.jpg 300w" sizes="(max-width: 766px) 100vw, 766px" /></noscript></figure> 346</div> 347 348 349 350<div class="wp-block-column"> 351<p>Childhood maltreatment exposure (CME) increases the risk of adverse long-term health consequences for the exposed individual. Animal studies suggest that CME may also influence the health and behaviour in the next generation offspring through CME-driven epigenetic changes in the germ line. Here we investigated the associated between early life stress on the epigenome of sperm in humans with history of CME. We measured paternal CME using the Trauma and Distress Scale (TADS) questionnaire and mapped sperm-borne sncRNAs expression by small RNA sequencing (small RNA-seq) and DNA methylation (DNAme) in spermatozoa by reduced-representation bisulfite sequencing (RRBS-seq) in males from the FinnBrain Birth Cohort Study. The study design was a (nested) case-control study, high-TADS (TADSââ¥â39, <em>n</em>â=â25 for DNAme and <em>n</em>â=â14 for small RNA-seq) and low-TADS (TADSââ¤â10, <em>n</em>â=â30 for DNAme and <em>n</em>â=â16 for small RNA-seq). We identified 3 genomic regions with differential methylation between low and high-TADS and 68 tRNA-derived small RNAs (tsRNAs) and miRNAs with different levels in males with high CME (False discovery rate, FDR corrected <em>p</em>â<â0.05). Of potential interest, we identified differential expression of miRNA hsa-mir-34c-5p and differential methylation levels near the <em>CRTC1</em> and <em>GBX2</em> genes, which are documented to control brain development. Our results provide further evidence that early life stress influences the paternal germline epigenome and supports a possible effect in modulating the development of the central nervous system of the next generation.</p> 352</div> 353</div> 354</div> 355</div> 356</div> 357</div> 358</div> 359</div> 360 361 362 363<hr class="wp-block-separator"/> 364 365 366 367<p></p> 368 369 370 371<h2 class="has-luminous-vivid-orange-color has-text-color" style="font-size:45px">2024</h2> 372 373 374 375<h3><strong>Extracellular vesicles – small messengers with a wide range of applications?</strong></h3> 376 377 378 379<p>Hufnagel A, Barrès R. <strong>Dan Med J</strong> 2024 Jul; 71(8)</p> 380 381 382 383<p class="has-vivid-cyan-blue-color has-text-color"><a href="https://ugeskriftet.dk/dmj/extracellular-vesicles-small-messengers-wide-range-applications" target="_blank" rel="noreferrer noopener"><em>https://ugeskriftet.dk/dmj/extracellular-vesicles-small-messengers-wide-range-applications</em></a></p> 384 385 386 387<div class="wp-block-columns"> 388<div class="wp-block-column" style="flex-basis:100%"> 389<div class="wp-block-columns"> 390<div class="wp-block-column" style="flex-basis:100%"> 391<div class="wp-block-columns"> 392<div class="wp-block-column"> 393<p>Extracellular vesicles (EVs) are small membranous vesicles secreted by many different cell types that have emerged as potentially important mediators of organ crosstalk. EVs are of research interest in health and disease and as biomarkers and therapeutic agents in various fields, including metabolism, reproduction, cancer, and others. Despite promising data and a growing understanding of their role, challenges and limitations of EV research remain, leaving room for optimisation regarding methods for pure isolations of EVs and translation into clinical practice.</p> 394</div> 395 396 397 398<div class="wp-block-column"> 399<figure class="wp-block-image size-large is-resized"><img src="data:image/svg+xml,%3Csvg%20xmlns='http://www.w3.org/2000/svg'%20viewBox='0%200%20339%20286'%3E%3C/svg%3E" alt="" class="wp-image-585" width="339" height="286" data-lazy-srcset="https://geckoconsortium.com/wp-content/uploads/2025/09/EV-image.png 472w, https://geckoconsortium.com/wp-content/uploads/2025/09/EV-image-300x254.png 300w" data-lazy-sizes="(max-width: 339px) 100vw, 339px" data-lazy-src="https://geckoconsortium.com/wp-content/uploads/2025/09/EV-image.png" /><noscript><img src="https://geckoconsortium.com/wp-content/uploads/2025/09/EV-image.png" alt="" class="wp-image-585" width="339" height="286" srcset="https://geckoconsortium.com/wp-content/uploads/2025/09/EV-image.png 472w, https://geckoconsortium.com/wp-content/uploads/2025/09/EV-image-300x254.png 300w" sizes="(max-width: 339px) 100vw, 339px" /></noscript></figure> 400</div> 401</div> 402</div> 403</div> 404</div> 405</div> 406 407 408 409<hr class="wp-block-separator"/> 410 411 412 413<p></p> 414 415 416 417<h3><strong>Epigenetics of the non-coding RNA nc886 across blood, adipose tissue and skeletal muscle in offspring exposed to diabetes in pregnancy.</strong></h3> 418 419 420 421<p>Hjort L, Bredgaard SS, Manitta E, Marques I, Sørensen AE, Martino D, Grunnet LG, Kelstrup L, Houshmand-Oeregaard A, Dalsgaard Clausen T, Mathiesen ER, Olsen SF, Saffery R, Barrès R, Damm P, Vaag AV, Dalgaard LT. <strong>Clinical Epigenetics</strong>. 2024 May 7;16(1):61.</p> 422 423 424 425<h3>
425Background</h3> 426 427 428 429<p>Diabetes in pregnancy is associated with increased risk of long-term metabolic disease in the offspring, potentially mediated by in utero epigenetic variation. Previously, we identified multiple differentially methylated single CpG sites in offspring of women with gestational diabetes mellitus (GDM), but whether stretches of differentially methylated regions (DMRs) can also be identified in adolescent GDM offspring is unknown. Here, we investigate which DNA regions in adolescent offspring are differentially methylated in blood by exposure to diabetes in pregnancy. The secondary aim was to characterize the RNA expression of the identified DMR, which contained the <em>nc886</em> non-coding RNA.</p> 430 431 432 433<h3>Methods</h3> 434 435 436 437<p>To identify DMRs, we employed the bump hunter method in samples from young (9â16 yr, <em>n</em>â=â92) offspring of women with GDM (O-GDM) and control offspring (<em>n</em>â=â94). Validation by pyrosequencing was performed in an adult offspring cohort (age 28â33 years) consisting of O-GDM (<em>n</em>â=â82), offspring exposed to maternal type 1 diabetes (O-T1D, <em>n</em>â=â67) and control offspring (O-BP, <em>n</em>â=â57). RNA-expression was measured using RT-qPCR in subcutaneous adipose tissue and skeletal muscle.</p> 438 439 440 441<h3>Results</h3> 442 443 444 445<p>One significant DMR represented by 10 CpGs with a bimodal methylation pattern was identified, located in the <em>nc886</em>/<em>VTRNA2-1</em> non-coding RNA gene. Low methylation status across all CpGs of the <em>nc886</em> in the young offspring was associated with maternal GDM. While low methylation degree in adult offspring in blood, adipose tissue, and skeletal muscle was not associated with maternal GDM, adipose tissue <em>nc886</em> expression was increased in O-GDM compared to O-BP, but not in O-T1D. In addition, adipose tissue <em>nc886</em> expression levels were positively associated with maternal pre-pregnancy BMI (<em>p</em>â=â0.006), but not with the offspringâs own adiposity.</p> 446 447 448 449<h3>Conclusions</h3> 450 451 452 453<p>Our results highlight that <em>nc886</em> is a metastable epiallele, whose methylation in young offspring is negatively correlated with maternal obesity and GDM status. The physiological effect of <em>nc886</em> may be more important in adipose tissue than in skeletal muscle. Further research should aim to investigate how <em>nc886</em> regulation in adipose tissue by exposure to GDM may contribute to development of metabolic disease.</p> 454 455 456 457<p class="has-vivid-cyan-blue-color has-text-color"><a href="https://clinicalepigeneticsjournal.biomedcentral.com/articles/10.1186/s13148-024-01673-3" target="_blank" rel="noreferrer noopener"><em>https://clinicalepigeneticsjournal.biomedcentral.com/articles/10.1186/s13148-024-01673-3</em></a></p> 458 459 460 461<hr class="wp-block-separator"/> 462 463 464 465<p></p> 466 467 468 469<h3><strong>Paternal dietary macronutrient balance and energy intake drive metabolic and behavioral differences among offspring</strong></h3> 470 471 472 473<p>Crean AJ, Senior AM, Freire T, Clark TD, Mackay F, Austin G, Pulpitel TJ, Nobrega MA, Barrès R, Simpson SJ., <strong>Nat Commun</strong> 2024 Apr; 15(1): 2982.</p> 474 475 476 477<p class="has-vivid-cyan-blue-color has-text-color"><a href="https://www.nature.com/articles/s41467-024-46782-y/figures/1" target="_blank" rel="noreferrer noopener"><em>https://www.nature.com/articles/s41467-024-46782-y/figures/1</em></a></p> 478 479 480 481<div class="wp-block-columns"> 482<div class="wp-block-column" style="flex-basis:100%"> 483<div class="wp-block-columns"> 484<div class="wp-block-column"> 485<figure class="wp-block-image size-large"><img width="1024" height="500" src="data:image/svg+xml,%3Csvg%20xmlns='http://www.w3.org/2000/svg'%20viewBox='0%200%201024%20500'%3E%3C/svg%3E" alt="" class="wp-image-588" data-lazy-srcset="https://geckoconsortium.com/wp-content/uploads/2025/09/crean-et-al-illustr-1024x500.png 1024w, https://geckoconsortium.com/wp-content/uploads/2025/09/crean-et-al-illustr-300x146.png 300w, https://geckoconsortium.com/wp-content/uploads/2025/09/crean-et-al-illustr-768x375.png 768w, https://geckoconsortium.com/wp-content/uploads/2025/09/crean-et-
485al-illustr.png 1107w" data-lazy-sizes="(max-width: 1024px) 100vw, 1024px" data-lazy-src="https://geckoconsortium.com/wp-content/uploads/2025/09/crean-et-al-illustr-1024x500.png" /><noscript><img width="1024" height="500" src="https://geckoconsortium.com/wp-content/uploads/2025/09/crean-et-al-illustr-1024x500.png" alt="" class="wp-image-588" srcset="https://geckoconsortium.com/wp-content/uploads/2025/09/crean-et-al-illustr-1024x500.png 1024w, https://geckoconsortium.com/wp-content/uploads/2025/09/crean-et-al-illustr-300x146.png 300w, https://geckoconsortium.com/wp-content/uploads/2025/09/crean-et-al-illustr-768x375.png 768w, https://geckoconsortium.com/wp-content/uploads/2025/09/crean-et-al-illustr.png 1107w" sizes="(max-width: 1024px) 100vw, 1024px" /></noscript></figure> 486</div> 487 488 489 490<div class="wp-block-column"> 491<p>Paternal diet can influence the phenotype of the next generation, yet, the dietary components inducing specific responses in the offspring are not identified. Here, we use the Nutritional Geometry Framework to determine the effects of pre-conception paternal dietary macronutrient balance on offspring metabolic and behavioral traits in mice. Ten isocaloric diets varying in the relative proportion of protein, fats, and carbohydrates are fed to male mice prior to mating. Dams and offspring are fed standard chow and never exposed to treatment diets. Body fat in female offspring is positively associated with the paternal consumption of fat, while in male offspring, an anxiety-like phenotype is associated to paternal diets low in protein and high in carbohydrates. Our study uncovers that the nature and the magnitude of paternal effects are driven by interactions between macronutrient balance and energy intake and are not solely the result of over- or undernutrition.</p> 492</div> 493</div> 494</div> 495</div> 496 497 498 499<hr class="wp-block-separator"/> 500 501 502 503<p></p> 504 505 506 507<h3><strong>Dietary macronutrient composition impacts gene regulation in adipose tissue</strong></h3> 508 509 510 511<p>Farris KM, Senior AM, Sobreira DR, Mitchell RM, Weber ZT, Ingerslev LR, Barrès R, Simpson SJ, Crean AJ, Nobrega MA, <strong>Commun Biol</strong> 2024 Feb; 7(1): 194.</p> 512 513 514 515<p class="has-vivid-cyan-blue-color has-text-color"><a href="https://www.nature.com/articles/s42003-024-05876-5" target="_blank" rel="noreferrer noopener"><em>https://www.nature.com/articles/s42003-024-05876-5</em></a></p> 516 517 518 519<p>Diet is a key lifestyle component that influences metabolic health through several factors, including total energy intake and macronutrient composition. While the impact of caloric intake on gene expression and physiological phenomena in various tissues is well described, the influence of dietary macronutrient composition on these parameters is less well studied. Here, we use the Nutritional Geometry framework to investigate the role of macronutrient composition on metabolic function and gene regulation in adipose tissue. Using ten isocaloric diets that vary systematically in their proportion of energy from fat, protein, and carbohydrates, we find that gene expression and splicing are highly responsive to macronutrient composition, with distinct sets of genes regulated by different macronutrient interactions. Specifically, the expression of many genes associated with Bardet-Biedl syndrome is responsive to dietary fat content. Splicing and expression changes occur in largely separate gene sets, highlighting distinct mechanisms by which dietary composition influences the transcriptome and emphasizing the importance of considering splicing changes to more fully capture the gene regulation response to environmental changes such as diet. Our study provides insight into the gene regulation plasticity of adipose tissue in response to macronutrient composition, beyond the already well-characterized response to caloric intake.</p> 520 521 522 523<hr class="wp-block-separator"/> 524 525 526 527<p class="has-vivid-cyan-blue-color has-text-color"></p> 528 529 530 531<h2 class="has-luminous-vivid-orange-color has-text-color" style="font-size:45px">2023</h2> 532 533 534 535<h3><strong>Splicing across adipocyte differentiation is highly dynamic and impacted by metabolic phenotype in adipose tissue</strong></h3> 536 537 538 539<p>Nobrega M, Farris K, Andersen E, Donkin I, Versteyhe S, Kristiansen VB, Simpson S, Barres R, <strong>Res Sq</strong> 2023 Oct</p> 540 541 542 543<p class="has-vivid-cyan-blue-color has-text-color"><a href="https://www.researchsquare.com/article/rs-3487148/v1" target="_blank" rel="noreferrer noopener">https://<em>www.researchsquare.com/article/rs-3487148/v1</em></a></p> 544 545 546 547<p>Adipose tissue dysfunction underlies many of the metabolic complications associated with obesity. A better understanding of the gene regulation differences present in metabolically unhealthy adipose tissue can provide insights into the mechanisms underlying adipose tissue dysfunction. Here, we used RNA-seq data collected from a differentiation time course of lean, obese, and obese with type 2 diabetes (T2D) individuals to characterize the role of alterative splicing in adipocyte differentiation and function. We found that splicing was highly dynamic across adipocyte differentiation in all three cohorts, and that the dynamics of splicing were significantly impacted by metabolic phenotype. We also found that there was very little overlap between genes that were differentially spliced in adipocyte differentiation and those that were differentially expressed, positioning alternative splicing as a largely independent gene regulatory mechanism whose impact would be missed when looking at gene expression changes alone. To assess the impact of alternative splicing across adipocyte differentiation on genetic risk for metabolic diseases, we integrated the differential splicing results generated here with genome-wide association study results for body mass index and T2D, and found that variants associated with T2D were enriched in regions that were differentially spliced in early differentiation. These findings provide insight into the role of alternative splicing in adipocyte differentiation and can serve as a resource to guide future variant-to-function studies.</p> 548 549 550 551<hr class="wp-block-separator"/> 552 553 554 555<p></p> 556 557 558 559<h3><strong>Male reproductive traits are differentially affected by dietary macronutrient balance but unrelated to adiposity</strong></h3> 560 561 562 563<p>A. Crean, S. Afrin, H. Niranjan, T. Pulpitel, G. Ahmad, A. Senior, T. Freire, F. Mackay, M. Nobrega, R. Barrès, S. Simpson, T. Pini, <strong>Nature Communications</strong>, 2023, 14 (1), pp.2566. â¨10.1038/s41467-023-38314-xâ©.</p> 564 565 566 567<p class="has-vivid-cyan-blue-color has-text-color"><a href="https://www.nature.com/articles/s41467-023-38314-x" target="_blank" rel="noreferrer noopener"><em>https://www.nature.com/articles/s41467-023-38314-x</em></a></p> 568 569 570 571<p>Dietary factors influence male reproductive function in both experimental and epidemiological studies. However, there are currently no specific dietary guidelines for male preconception health. Here, we use the Nutritional Geometry framework to examine the effects of dietary macronutrient balance on reproductive traits in C57BL/6âJ male mice. Dietary effects are observed in a range of morphological, testicular and spermatozoa traits, although the relative influence of protein, fat, carbohydrate, and their interactions differ depending on the trait being examined. Interestingly, dietary fat has a positive influence on sperm motility and antioxidant capacity, differing to typical high fat diet studies where calorie content is not controlled for. Moreover, body adiposity is not significantly correlated with any of the reproductive traits measured in this study. These results demonstrate the importance of macronutrient balance and calorie intake on reproductive function and support the need to develop specific, targeted, preconception dietary guidelines for males.</p> 572 573 574 575<hr class="wp-block-separator"/> 576 577 578 579<p></p> 580 581 582 583<h3 class="has-luminous-vivid-orange-color has-text-color" style="font-size:45px">2022</h3> 584 585 586 587<h3><strong>Comparative analysis of sperm DNA methylation supports evolutionary acquired epigenetic plasticity for organ speciation</strong></h3> 588 589 590 591<p>Moharrek F, Ingerslev LR, AltıntaÅ A, Lundell L, Hansen AN, Small L, Workman CT and Barrès R. <strong>Epigenomics</strong>. 2022 Nov 24. doi: 10.2217/epi-2022-0168<em>.</em></p> 592 593 594 595<p><strong>Aim:</strong> To perform a comparative epigenomic analysis of DNA methylation in spermatozoa from humans, mice, rats and mini-pigs. <strong>Materials & methods:</strong> Genome-wide DNA methylation analysis was used to compare the methylation profiles of orthologous CpG sites. Transcription profiles of early embryo development were analyzed to provide insight into the association between sperm methylation and gene expression programming. <strong>Results:</strong> We identified DNA methylation variation near genes related to the central nervous system and signal transduction. Gene expression dynamics at different time points of preimplantation stages were modestly associated with spermatozoal DNA methylation at the nearest promoters. <strong>Conclusion:</strong> Conserved genomic regions subject to epigenetic variation across different species were associated with specific organ functions, suggesting their potential contribution to organ speciation and long-term adaptation to the environment.</p> 596 597 598 599<p class="has-vivid-cyan-blue-color has-text-color"><em><a href="https://www.tandfonline.com/doi/10.2217/epi-2022-0168?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed" target="_blank" rel="noreferrer noopener">https://www.tandfonline.com/doi/10.2217/epi-2022-0168?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed</a></em></p> 600 601 602 603<hr class="wp-block-separator"/> 604 605 606 607<p></p> 608 609 610 611<h3><strong>DNA methylation and gene expression in blood and adipose tissue of adult offspring of women with diabetes in pregnancy â A validation study of DNA methylation changes identified in adolescent offspring</strong></h3> 612 613 614 615<p>Manitta E, Marques ICF, Stokholm S, Kelstrup BL, Houshmand-Oeregaard A, Clausen DT, Grunnet LG, Mathiesen ER, Dalgaard LT, Barrès R, Vaag AA, Damm P, Hjort L. <strong>Biomedicines</strong>. 2022 May 26;10(6):1244.</p> 616 617 618 619<p>Maternal gestational diabetes and obesity are associated with adverse outcomes in offspring, including increased risk of diabetes and cardiovascular diseases. Previously, we identified a lower DNA methylation degree at genomic sites near the genes ESM1, MS4A3, and TSPAN14 in the blood cells of adolescent offspring exposed to gestational diabetes and/or maternal obesity in utero. In the present study, we aimed to investigate if altered methylation and expression of these genes were detectable in blood, as well in the metabolically relevant subcutaneous adipose tissue, in a separate cohort of adult offspring exposed to gestational diabetes and obesity (O-GDM) or type 1 diabetes (O-T1D) in utero, compared with the offspring of women from the background population (O-BP). We did not replicate the findings of lower methylation of ESM1, MS4A3, and TSPAN14 in blood from adults, either in O-GDM or O-T1D. In contrast, in adipose tissue of O-T1D, we found higher MS4A3 DNA methylation, which will require further validation. The adipose tissue ESM1 expression was lower in O-GDM compared to O-BP, which in turn was not associated with maternal pre-pregnancy BMI nor the offspringâs own adiposity. Adipose tissue TSPAN14 expression was slightly lower in O-GDM compared with O-BP, but also positively associated with maternal pre-pregnancy BMI, as well as offspringâs own adiposity and HbA1c levels. In conclusion, the lower DNA methylation in blood from adolescent offspring exposed to GDM could not be confirmed in the present cohort of adult offspring, potentially due to methylation remodeling with increased aging. In offspring adipose tissue, ESM1 expression was associated with maternal GDM, and TSPAN14 expression was associated with both maternal GDM, as well as pre-pregnancy BMI. These altered expression patterns are potentially relevant to the concept of developmental programming of cardiometabolic diseases and require further studies.</p> 620 621 622 623<p class="has-vivid-cyan-blue-color has-text-color"><em><a href="https://www.mdpi.com/2227-9059/10/6/1244" target="_blank" rel="noreferrer noopener">https://www.mdpi.com/2227-9059/10/6/1244</a></em></p> 624 625 626 627<hr class="wp-block-separator"/> 628 629 630 631<p></p> 632 633 634 635<h3><strong>Sperm count is increased by diet-induced weight loss and maintained by exercise or GLP-1 analogue treatment: a randomised controlled trial</strong></h3> 636 637 638 639<p>Andersen E, Juhl CR, Kjøller ET, Lundgren JR, Janus C, Dehestani Y, Saupstad M, Ingerslev LR, Duun OR, Jensen SBK, Holst JJ, Stallknecht BM, Madsbad S, Torekov SS, Barrès R. <strong>Human Reproduction</strong>. 2022 May 17:deac096.</p> 640 641 642 643<p>STUDY QUESTION</p> 644 645 646 647<p>Does diet-induced weight loss improve semen parameters, and are these possible improvements maintained with sustained weight loss?</p> 648 649 650 651<p>SUMMARY ANSWER</p> 652 653 654 655<p>An 8-week low-calorie diet-induced weight loss was associated with improved sperm concentration and sperm count, which were maintained after 1 year in men who maintained weight loss.</p> 656 657 658 659<p>WHAT IS KNOWN ALREADY</p> 660 661 662 663<p>Obesity is associated with impaired semen quality. Weight loss improves metabolic health in obesity, but there is a lack of knowledge on the acute and long-term effects of weight loss on semen parameters.</p> 664 665 666 667<p>STUDY DESIGN, SIZE, DURATION</p> 668 669 670 671<p>This is a substudy of men with obesity enrolled in a randomized, controlled, double-blinded trial (the S-LITE trial). The trial was conducted between August 2016 and November 2019. A total of 56 men were included in the study and assigned to an initial 8-week low-calorie diet (800âkcal/day) followed by randomization to 52âweeks of either: placebo and habitual activity (placebo), exercise training and placebo (exercise), the Glucagon Like Peptide 1 (GLP-1) analogue liraglutide and habitual activity (liraglutide) or liraglutide in combination with exercise training (combination).</p> 672 673 674 675<figure class="wp-block-image size-large"><img width="626" height="268" src="data:image/svg+xml,%3Csvg%20xmlns='http://www.w3.org/2000/svg'%20viewBox='0%200%20626%20268'%3E%3C/svg%3E" alt="" class="wp-image-617" data-lazy-srcset="https://geckoconsortium.com/wp-content/uploads/2025/09/Capture-decran-2025-09-17-143322.jpg 626w, https://geckoconsortium.com/wp-content/uploads/2025/09/Capture-decran-2025-09-17-143322-300x128.jpg 300w" data-lazy-sizes="(max-width: 626px) 100v
675w, 626px" data-lazy-src="https://geckoconsortium.com/wp-content/uploads/2025/09/Capture-decran-2025-09-17-143322.jpg" /><noscript><img width="626" height="268" src="https://geckoconsortium.com/wp-content/uploads/2025/09/Capture-decran-2025-09-17-143322.jpg" alt="" class="wp-image-617" srcset="https://geckoconsortium.com/wp-content/uploads/2025/09/Capture-decran-2025-09-17-143322.jpg 626w, https://geckoconsortium.com/wp-content/uploads/2025/09/Capture-decran-2025-09-17-143322-300x128.jpg 300w" sizes="(max-width: 626px) 100vw, 626px" /></noscript></figure> 676 677 678 679<p>PARTICIPANTS/MATERIALS, SETTING, METHODS</p> 680 681 682 683<p>Inclusion criteria were men who delivered semen samples, 18 to 65âyears of age, and a body mass index between 32 and 43âkg/m<sup>2</sup>, but otherwise healthy. The study was carried out at Hvidovre Hospital and at the University of Copenhagen, and the participants were from the Greater Copenhagen Area. We assessed semen parameters and anthropometrics and collected blood samples before (T0), after the 8-week low-calorie dietary intervention (T1), and after 52âweeks (T2).</p> 684 685 686 687<p>MAIN RESULTS AND THE ROLE OF CHANCE</p> 688 689 690 691<p>The men lost on average 16.5âkg (95% CI: 15.2â17.8) body weight during the low-calorie diet, which increased sperm concentration 1.49-fold (95% CI: 1.18â1.88, <em>Pâ</em><0.01) and sperm count 1.41-fold (95% CI: 1.07â1.87, <em>Pâ</em><0.01). These improvements were maintained for 52âweeks in men who maintained the weight loss, but not in men who regained weight. Semen volume, sperm motility and motile sperm count did not change.LIMITATIONS, REASONS FOR CAUTION</p> 692 693 694 695<p>The S-LITE trial was a randomized controlled trial of weight loss maintenance. Analysis of semen was preregistered to explore the effects of weight loss and weight loss maintenance on semen parameters, but definite inferences cannot be made.</p> 696 697 698 699<p>WIDER IMPLICATIONS OF THE FINDINGS</p> 700 701 702 703<p>This study shows that sperm concentration and sperm count were improved after a diet-induced weight loss in men with obesity. Our findings indicate that either or both liraglutide and exercise as weight maintenance strategies may be used to maintain the improvements in sperm concentration and count.STUDY FUNDING/COMPETING INTEREST(S)</p> 704 705 706 707<p>This work is supported by an excellence grant from the Novo Nordisk Foundation (NNF16OC0019968), a Challenge Programme Grant from the Novo Nordisk Foundation (NNF18OC0033754) and a grant from Helsefonden. The Novo Nordisk Foundation Center for Basic Metabolic Research is an independent research centre at the University of Copenhagen, partially funded by an unrestricted donation from the Novo Nordisk Foundation (NNF18CC0034900). Saxenda (liraglutide) and placebo pens were provided by Novo Nordisk. Cambridge Weight Plan diet products for the 8-week low-calorie diet were provided by Cambridge Weight Plan. E.A.: shareholder, employee of ExSeed Health Ltd. Grant Recipient from ExSeed Health Ltd and listed on Patents planned, issued or pending with ExSeed Health Ltd; J.J.H.: consultant for Eli Lilly A/S and Novo Nordisk A/S. Lecture fees for Novo Nordisk A/S. Listed on Patents planned, issued or pending with the University of Copenhagen, Advocacy group for Antag Therapeutics and Bainan Biotech; S.M.: lecture fees for Novo Nordisk A/S. Recipient of Support for attending meetings from Novo Nordisk A/S. Advisory boards of Novo Nordisk A/S; Sanofi Aventis and Merck Sharp & Dohme. S.S.T.: research grant recipient Novo Nordisk. The remaining authors have no conflicts of interest to declare.</p> 708 709 710 711<p>TRIAL REGISTRATION NUMBER</p> 712 713 714 715<p>The trial was approved by the Ethical Committee of the Capital Region of Denmark (H-16027082) and the Danish Medicines Agency (EudraCT Number: 2015-005585-32). ClinicalTrials.gov identifier (NCT number): NCT04122716.</p> 716 717 718 719<p>TRIAL REGISTRATION DATE</p> 720 721 722 723<p>11 May 2016.</p> 724 725 726 727<p>DATE OF FIRST PATIENTâS ENROLMENT</p> 728 729 730 731<p>August 2016.</p> 732 733 734 735<p class="has-vivid-cyan-blue-color has-text-color"><em><a href="https://academic.oup.com/humrep/article/37/7/1414/6587152?login=true" target="_blank" rel="noreferrer noopener">https://academic.oup.com/humrep/article/37/7/1414/6587152?login=true</a></em></p> 736 </div> 737 </div> 738 </div> 739 </article> 740 741 742 </section><!-- #primary --> 743 </main><!-- #main --> 744 745<!-- footer --> 746<footer class="footer" role="contentinfo" data-anim="fade-slide-up"> 747 748 <div class="container"> 749 <div class="row footer-about"> 750 <!-- copyright --> 751 <div class="small-12 medium-4 large-4 columns about-company"> 752 <img width="356" height="89" 753 src="data:image/svg+xml,%3Csvg%20xmlns='http://www.w3.org/2000/svg'%20viewBox='0%200%20356%2089'%3E%3C/svg%3E" 754 alt="Logo" class="logo-big" data-lazy-src="https://geckoconsortium.com/wp-content/themes/gecko/assets/images/logo-big.svg"><noscript><img width="356" height="89" 755 src="https://geckoconsortium.com/wp-content/themes/gecko/assets/images/logo-big.svg" 756 alt="Logo" class="logo-big"></noscript> 757 <p>GECKO is an international consortium of researchers working to understand the ancestral causes of obesity</p> 758 </div> 759 <!-- /copyright --> 760 761 <!-- powered by --> 762 <div class="small-12 medium-3 large-2 columns footer-menu-wrap"> 763 <h4>About</h4> 764 <ul id="footer-menu" class="footer-menu"><li id="menu-item-129" class="menu-item menu-item-type-post_type menu-item-object-page menu-item-129"><a href="https://geckoconsortium.com/consortium-members/">Consortium</a></li> 765<li id="menu-item-127" class="menu-item menu-item-type-post_type menu-item-object-page menu-item-127"><a href="https://geckoconsortium.com/contact/">Contact</a></li> 766<li id="menu-item-128" class="menu-item menu-item-type-post_type menu-item-object-page menu-item-128"><a href="https://geckoconsortium.com/about-gecko/">About GECKO</a></li> 767<li id="menu-item-132" class="menu-item menu-item-type-post_type menu-item-object-page menu-item-privacy-policy menu-item-132"><a href="https://geckoconsortium.com/privacy-policy/">Privacy Policy</a></li> 768<li id="menu-item-332" class="menu-item menu-item-type-post_type menu-item-object-page menu-item-332"><a href="https://geckoconsortium.com/cookie-policy/">Cookie Policy</a></li> 769</ul> </div> 770 <!-- /powered by --> 771 772 <!-- powered by --> 773 <div class="small-12 medium-4 large-3 columns footer-foundation"> 774 <h4>Funded by Novo Nordisk Foundation</h4> 775 <p>We are funded by a Novo Nordisk Foundation Challenge Grant 33754 from 2019 â 2025.</p> 776 <div class="footer-social"> 777 <h4>Follow on social media</h4> 778 <ul class="footer-social__list"> 779 <li class="footer-social__item"> 780 <a href="https://twitter.com/geckoconsortium" target="_blank"> 781 <svg class="icon ixon-twitter-x" xmlns="http://www.w3.org/2000/svg" width="24" height="24" viewBox="0 0 24 24">
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928<script src='https://geckoconsortium.com/wp-includes/js/wp-embed.min.js?ver=5.7.2.1699270096' id='wp-embed-js'></script>
vendor: 1 bytes, line 928
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929<script>window.lazyLoadOptions={elements_selector:"img[data-lazy-src],.rocket-lazyload,iframe[data-lazy-src]",data_src:"lazy-src",data_srcset:"lazy-srcset",data_sizes:"lazy-sizes",class_loading:"lazyloading",class_loaded:"lazyloaded",threshold:300,callback_loaded:function(element){if(element.tagName==="IFRAME"&&element.dataset.rocketLazyload=="fitvidscompatible"){if(element.classList.contains("lazyloaded")){if(typeof window.jQuery!="undefined"){if(jQuery.fn.fitVids){jQuery(element).parent().fitVids()}}}}}};window.addEventListener('LazyLoad::Initialized',function(e){var lazyLoadInstance=e.detail.instance;if(window.MutationObserver){var observer=new MutationObserver(function(mutations){var image_count=0;var iframe_count=0;var rocketlazy_count=0;mutations.forEach(function(mutation){for(i=0;i<mutation.addedNodes.length;i++){if(typeof mutation.addedNodes[i].getElementsByTagName!=='function'){continue} 930if(typeof mutation.addedNodes[i].getElementsByClassName!=='function'){continue} 931images=mutation.addedNodes[i].getElementsByTagName('img');is_image=mutation.addedNodes[i].tagName=="IMG";iframes=mutation.addedNodes[i].getElementsByTagName('iframe');is_iframe=mutation.addedNodes[i].tagName=="IFRAME";rocket_lazy=mutation.addedNodes[i].getElementsByClassName('rocket-lazyload');image_count+=images.length;iframe_count+=iframes.length;rocketlazy_count+=rocket_lazy.length;if(is_image){image_count+=1} 932if(is_iframe){iframe_count+=1}}});if(image_count>0||iframe_count>0||rocketlazy_count>0){lazyLoadInstance.update()}});var b=document.getElementsByTagName("body")[0];var config={childList:!0,subtree:!0};observer.observe(b,config)}},!1)</script>
932<script data-no-minify="1" async src="https://geckoconsortium.com/wp-content/plugins/wp-rocket/assets/js/lazyload/16.1/lazyload.min.js"></script>
932 933</body> 934</html> 935<!-- This website is like a Rocket, isn't it? Performance optimized by WP Rocket. Learn more: https://wp-rocket.me - Debug: cached@1791116082 -->
Line numbers count LF bytes from the start of the resource, as the search results do. Vendor segments are library code the classifier recognised; they are stored but not indexed. Bytes are shown as Latin1 characters, one per byte.