Fat Mass Accumulation Research Articles

Combined oral contraceptive use and obesity in women with polycystic ovary syndrome. A meta-analysis of randomized clinical trials.

Polycystic ovary syndrome (PCOS) is a heterogenous endocrine condition and combined oral contraceptives (COCs) have been demonstrated to be the first-line treatment to women who do not intend to become pregnant. The combination of COCs and PCOS may or may not amplify the risks of cardiovascular events. To investigate whether surrogates for obesity may be influenced by the use of COCs containing different formulations in women with PCOS. From January 2024 a literature search was conducted in Google Scholar and Pubmed databases using PCOS, COC, and obesity terms. Hand search of randomized clinical trials in the references of obtained manuscripts was also performed. After the exclusion of reviews and articles that did not fulfill eligibility criteria, compared the results obtained before and after the use of COCs in 13 randomized clinical trials (RCTs). Random-effects model was used to estimate the standardized mean differences (SMD) and standard errors (SE). Risk of bias was examined using the Rob2 tool. Thirteen heterogeneous RCTs reported no difference in waist circumference with the use of different COC formulations (p = 0.714). On the contrary, body fat mass increased with the use of pill (p = 0.013). Waist triglyceride index and lipid accumulation product tended to be higher after the use of COCs (p = 0.073 and p = 0.064, respectively). Combined oral contraceptives with different formulations might increase fat mass accumulation in women with PCOS. Lipids may also be increased in PCOS users. Because some concerns about the quality and heterogeneity identified in various RCTs, caution should be taken before a definitive conclusion regarding the use of COCs and obesity.

Synergy between time-restricted feeding and time-restricted running is necessary to shift the muscle clock in male wistar rats

Circadian disruption is an important factor driving the current-day high prevalence of obesity and type-2 diabetes. While the impact of incorrect timing of caloric intake on circadian disruption is widely acknowlegded, the contribution of incorrect timing of physical activity remains relatively understudied. Here, we modeled the incorrect timing of physical activity in nightshift workers in male Wistar rats, by restricting running wheel access to the innate inactive (light) phase (LR). Controls included no wheel access (NR); access only during the innate active (dark) period (DR); or unrestricted (ad libitum) access (ALR). LR did not shift the phase of the muscle or liver clock, but dampened the muscle clock amplitude. As our previous study demonstrated that light-phase restricted feeding did shift the liver clock, but made the muscle clock arrhythmic, we next combined the time restriction of wheel and food access to either the light phase (LRLF) or dark phase (DRDF). LRLF produced a ∼12 h shift in the majority of clock gene rhythms in both skeletal muscle and liver. On the other hand, DRDF was most effective in reducing body weight and the accumulation of fat mass. Therefore, in order to shift the muscle clock in male Wistar rats, synergy between the timing of feeding and physical activity is necessary. These findings may contribute to further improve the design of lifestyle strategies that try to limit metabolic misalignment caused by circadian disruption.

Role of the intestinal microbiota in contributing to weight disorders and associated comorbidities.

SUMMARYThe gut microbiota is a major factor contributing to the regulation of energy homeostasis and has been linked to both excessive body weight and accumulation of fat mass (i.e., overweight, obesity) or body weight loss, weakness, muscle atrophy, and fat depletion (i.e., cachexia). These syndromes are characterized by multiple metabolic dysfunctions including abnormal regulation of food reward and intake, energy storage, and low-grade inflammation. Given the increasing worldwide prevalence of obesity, cachexia, and associated metabolic disorders, novel therapeutic strategies are needed. Among the different mechanisms explaining how the gut microbiota is capable of influencing host metabolism and energy balance, numerous studies have investigated the complex interactions existing between nutrition, gut microbes, and their metabolites. In this review, we discuss how gut microbes and different microbiota-derived metabolites regulate host metabolism. We describe the role of the gut barrier function in the onset of inflammation in this context. We explore the importance of the gut-to-brain axis in the regulation of energy homeostasis and glucose metabolism but also the key role played by the liver. Finally, we present specific key examples of how using targeted approaches such as prebiotics and probiotics might affect specific metabolites, their signaling pathways, and their interactions with the host and reflect on the challenges to move from bench to bedside.

Regimen on Dnaja3 haploinsufficiency mediated sarcopenic obesity with imbalanced mitochondrial homeostasis and lipid metabolism.

Sarcopenic obesity is characterized by excess fat mass and diminished muscular mass/function. DNAJA3, a mitochondrial co-chaperone protein, plays a crucial role in skeletal muscle development. GMI, an immunomodulatory protein, promotes myogenic differentiation through DNAJA3 activation. This study aims to elucidate the physiological effects of muscular Dnaja3 haploinsufficiency on mitochondrial dysfunction and dysregulated lipid metabolism and to assess the efficacy of GMI in rescuing sarcopenic obesity both in vitro and in vivo. We generated mouse strain with Dnaja3 heterozygosity (HSA-Dnaja3f/+) specifically in skeletal muscle. The body weight, body composition, and locomotor activity of WT and HSA-Dnaja3f/+ mice were examined. The isolated skeletal muscles and primary myoblasts from the WT and HSA-Dnaja3f/+ mice, at young or old age, were utilized to study the molecular mechanisms, mitochondrial respiration and ROS level, mitochondrial proteomes, and serological analyses, respectively. To evaluate the therapeutic efficacy of GMI, both short-term and long-term GMI treatment were administrated intraperitoneally to the HSA-Dnaja3f/+ young (4weeks old) or adult (3months old) mice for a duration of either 1 or 6months, respectively. Muscular Dnaja3 heterozygosity resulted in impaired locomotor activity (P<0.05), reduced muscular cross-sectional area (P<0.0001), and up-regulation of lipogenesis (ACC2) and pro-inflammation (STAT3) in skeletal muscles (P<0.05). Primary myoblasts from the HSA-Dnaja3f/+ mice displayed impaired mitochondrial respiration (P<0.01) and imbalanced mitochondrial ROS levels. A systemic proteomic analysis of the purified mitochondria from the primary myoblasts was conducted to show the abnormalities in mitochondrial function and fatty acid metabolism (P<0.0001). At age of 13 to 14months, the HSA-Dnaja3f/+ mice displayed increased body fat mass (P<0.001), reduced fat-free mass (P<0.01), and impaired glucose and insulin tolerance (P<0.01). The short-term GMI treatment improved locomotor activity (P<0.01) and down-regulated the protein levels of STAT3 (P<0.05), ACC2, and mitochondrial respiratory complex III (UQCRC2) (P<0.01) via DNAJA3 activation. The long-term GMI treatment ameliorated fat mass accumulation, glucose intolerance, and systemic inflammation (AST) (P<0.05) in skeletal muscle, while enhancing thermogenesis (UCP1) (P<0.01) in eWAT. GMI treatment promoted myogenesis, enhanced oxygen consumption, and ameliorated STAT3 (P<0.01) through DNAJA3 activation (P<0.05) in vitro. Muscular Dnaja3 haploinsufficiency dysregulates mitochondrial function and lipid metabolism then leads to sarcopenic obesity. GMI emerges as a therapeutic regimen for sarcopenic obesity treatment through DNAJA3 activation.

Olanzapine Modulate Lipid Metabolism and Adipose Tissue Accumulation via Hepatic Muscarinic M3 Receptor-Mediated Alk-Related Signaling.

Olanzapine is an atypical antipsychotic drug and a potent muscarinic M3 receptor (M3R) antagonist. Olanzapine has been reported to cause metabolic disorders, including dyslipidemia. Anaplastic lymphoma kinase (Alk), a tyrosine kinase receptor well known in the pathogenesis of cancer, has been recently identified as a key gene in the regulation of thinness via the regulation of adipose tissue lipolysis. This project aimed to investigate whether Olanzapine could modulate the hepatic Alk pathway and lipid metabolism via M3R. Female rats were treated with Olanzapine and/or Cevimeline (an M3R agonist) for 9 weeks. Lipid metabolism and hepatic Alk signaling were analyzed. Nine weeks' treatment of Olanzapine caused metabolic disturbance including increased body mass index (BMI), fat mass accumulation, and abnormal lipid metabolism. Olanzapine treatment also led to an upregulation of Chrm3, Alk, and its regulator Ptprz1, and a downregulation of Lmo4, a transcriptional repressor of Alk in the liver. Moreover, there were positive correlations between Alk and Chrm3, Alk and Ptprz1, and a negative correlation between Alk and Lmo4. However, cotreatment with Cevimeline significantly reversed the lipid metabolic disturbance and adipose tissue accumulation, as well as the upregulation of the hepatic Alk signaling caused by Olanzapine. This study demonstrates evidence that Olanzapine may cause metabolic disturbance by modulating hepatic Alk signaling via M3R, which provides novel insight for modulating the hepatic Alk signaling and potential interventions for targeting metabolic disorders.

Obesogenic diet induces sex-specific alterations of contextual fear memory and associated hippocampal activity in mice.

In addition to metabolic and cardiovascular disorders, obesity is associated with cognitive deficits in humans and animal models. We have previously shown that obesogenic high-fat and sugar diet intake during adolescence (adoHFSD) impairs hippocampus (HPC)-dependent memory in rodents. These results were obtained in males only and it remains to evaluate whether adoHFSD has similar effect in females. Therefore, here, we investigated the effects of adoHFSD consumption on HPC-dependent contextual fear memory and associated brain activation in male and female mice. Exposure to adoHFSD increased fat mass accumulation and glucose levels in both males and females but impaired contextual fear memory only in males. Compared with females, contextual fear conditioning induced higher neuronal activation in the dorsal and ventral HPC (CA1 and CA3 subfields) as well as in the medial prefrontal cortex in males. Also, adoHFSD-fed males showed enhanced c-Fos expression in the dorsal HPC, particularly in the dentate gyrus, and in the basolateral amygdala compared with the other groups. Finally, chemogenetic inactivation of the dorsal HPC rescued adoHFSD-induced memory deficits in males. Our results suggest that males are more vulnerable to the effects of adoHFSD on HPC-dependent aversive memory than females, due to overactivation of the dorsal HPC.

Asymmetry in Body Composition Variables of Youth Athletes

Assessing bilateral differences in paired anthropometric features is an important methodological problem in sports anthropology. The present study included 128 adolescent female athletes (59 rhythmic gymnasts, 58 tennis players, and 11 swimmers). Body composition components were determined using multi-frequency bioelectrical impedance measurements (analyzer InBody 170). Asymmetry coefficients of muscle and fat mass accumulation in the upper (AA) and lower (AL) limbs were calculated using the Nacheva` equation (1986). The percentiles method was applied to distribute the bilaterally studied anthropometric features according to the mean values of the units of asymmetry (UA). Wilkoxon-test was used to assess the statistically significant differences in paired variables. Kruskal-Wallis test was applied to determine the differences in UA between three assessed athlete groups, depending on their age. The differences in body composition components between rhythmic gymnasts (RG), tennis players (TP), and swimmers (SW) were well expressed in all assessed age groups. The most considerable inter-group differences were observed in terms of the asymmetry coefficient in the lean body mass (LBM) with a right direction and body fat mass with a left direction for upper limb fat mass (%, kg), which have signed the highest values in the tennis players group, followed by the RG on the same age. Swimmers had significantly the lowest values of UA for all body segments. A close relation was found between asymmetry in body composition variables and the type of sports activity. Tennis was found as a sport with more pronounced inter-limbs asymmetry.

Intestinal Acyl-CoA synthetase 5 (ACSL5) deficiency potentiates postprandial GLP-1 & PYY secretion, reduces food intake, and protects against diet-induced obesity

ObjectiveIn the small intestine, the products of digestion of dietary triacylglycerol (TAG), fatty acids (FA) and monoacylglycerol, are taken up by absorptive cells, enterocytes, for systemic energy delivery. These digestion products can also bind receptors on endocrine cells to stimulate the release of hormones capable of influencing systemic energy metabolism. The initial phase of intestinal FA absorption involves the acylation of FAs to acyl-CoA by the acyl-CoA long chain synthetase (ACSL) enzymes. ACSL5 is abundantly expressed in the small intestinal epithelium where it is the major ACSL isoform, contributing approximately 80% of total ACSL activity. In mice with whole body deficiency of ACSL5, the rate of dietary fat absorption is reduced and energy expenditure is increased. However, the mechanisms by which intestinal ACSL5 contributes to intestinal FA metabolism, enteroendocrine signaling, and regulation of energy expenditure remain undefined. Here, we test the hypothesis that intestinal ACSL5 regulates energy metabolism by influencing dietary fat absorption and enteroendocrine signaling. MethodsTo explore the role of intestinal ACSL5 in energy balance and intestinal dietary fat absorption, a novel mouse model of intestine specific ACSL5 deficiency (ACSL5IKO) was generated by breeding ACSL5 floxed (ACSL5loxP/loxP) to mice harboring the tamoxifen inducible, villin-Cre recombinase. ACSL5IKO and control, ACSL5loxP/loxP mice were fed chow (low in fat) or a 60% high fat diet (HFD), and metabolic phenotyping was performed including, body weight, body composition, insulin and glucose tolerance tests, energy expenditure, physical activity, and food intake studies. Pair-feeding studies were performed to determine the role of food intake in regulating development of obesity. Studies of dietary fat absorption, fecal lipid excretion, intestinal mucosal FA content, and circulating levels of glucagon like peptide 1 (GLP-1) and peptide YY (PYY) in response to a TAG challenge were performed. Treatment with a GLP-1 receptor antagonist was performed to determine the contribution of GLP-1 to acute regulation of food intake. ResultsWe found that ACSL5IKO mice experienced rapid and sustained protection from body weight and fat mass accumulation during HFD feeding. While intestine specific deficiency of ACSL5 delayed gastric emptying and reduced dietary fat secretion, it did not result in increased excretion of dietary lipid in feces. Energy expenditure and physical activity were not increased in ACSL5IKO mice. Mice deficient in intestinal ACSL5 display significantly reduced energy intake during HFD, but not chow feeding. When HFD intake of control mice was matched to ACSL5IKO during pair-feeding studies, no differences in body weight or fat mass gain were observed between groups. Postprandial GLP-1 and PYY were significantly elevated in ACSL5IKO mice secondary to increased FA content in the distal small intestine. Blockade of GLP-1 signaling by administration of a long-acting GLP-1 receptor antagonist partially restored HFD intake of ACSL5IKO. ConclusionsThese data indicate that intestinal ACSL5 serves as a critical regulator of energy balance, protecting mice from diet-induced obesity exclusively by increasing satiety and reducing food intake during HFD feeding. The reduction in food intake observed in ACSL5IKO mice is driven, in part, by increased postprandial GLP-1 and PYY secretion. These effects are only observed during HFD feeding, suggesting that altered processing of dietary fat following intestinal ACSL5 ablation contributes to GLP-1 and PYY mediated increases in satiety.

Maternal high‐fat diet associated with LPS gestational injection induces hypothalamic inflammation and metabolic disorders in male Wistar rat offspring

AbstractMaternal high‐fat diet (HFD) is linked to obesity and inflammation, predisposing offspring to metabolic and nutritional disorders. Accordingly, elevated blood levels of lipopolysaccharide (LPS) are also related to inflammation and metabolic complications in the offspring. The aim of this study was to evaluate the effects of the association of maternal HFD (gestation and lactation) and the LPS injection (gestation) on metabolic, inflammatory, and redox status parameters in male adolescent offspring. Female pregnant Wistar rats received randomly a standard or an HFD during gestation and lactation. On gestation Days 8, 10, and 12, half of the females in each group were intraperitonially injected with LPS (0.1 mg.kg−1). After weaning, all offspring received a standard diet. The dams and part of the male offspring were evaluated at weaning (Postnatal Day [PND] 21; food intake and inflammatory parameters), while the rest of the male offspring were evaluated during adolescence (PND50; food intake, redox status, and inflammatory parameters). HFD dams showed during gestation a lower weight gain. After lactation, HFD and LPS+HFD dams reported higher fat mass accumulation and increased interleukin‐6 (IL‐6) blood levels. HFD and LPS+HFD offspring showed at weaning higher levels of fat mass, body weight, and body length, besides an increased in hypothalamic IL‐6 levels. Noteworthy, at PND50, the LPS+HFD offspring showed higher energy intake, fat mass, and hypothalamic IL‐6 levels, in addition to an increased sucrose preference. Therefore, LPS+HFD offspring presented a worsening in energy metabolism, which was probably due to persistent hypothalamic inflammation, and also have a predisposition for the consumption of sweet foods.

Controlled expression of avian pre-migratory fattening influences indices of innate immunity.

While immunity is frequently dampened when birds engage in strenuous migratory flights, whether and how immunity changes during the rapid accumulation of energy stores in preparation for migration remains largely unknown. Here we induced pre-migratory fattening through controlled changes of daylight in common quails (Coturnix coturnix) and regularly assessed changes in three markers of constitutive innate immunity (leukocyte coping capacity or LCC, hemagglutination and hemolysis titres) and measures of body composition (lean and fat mass). All the three markers showed similar changes over the pre-migratory fattening process. LCC responses, hemagglutination titres, and hemolysis titres, were on average higher in the mid-fattening phase compared to the peak-fattening phase, when values were similar to those observed prior the start of pre-migratory fattening. At mid-fattening, we found that the birds that showed a larger accumulation of fat mass (as % of body mass) had lower LCC peak responses and hemolysis titres. Reversibly, at mid-fattening, we also found that the birds that kept a higher proportion of lean mass (as % of body mass) had the highest LCC peaks. Our results indicate that migratory birds undergo changes in immune indices (over 8 weeks) as they accumulate energy stores for migration and propose that this could be due to competing or trade-off processes between metabolic remodelling and innate immune system function.

Differences in segmental fat accumulation patterns by sex and ethnicity: An international approach.

Excess fat on the body impacts obesity-related co-morbidity risk; however, the location of fat stores affects the severity of these risks. The purpose of this study was to examine segmental fat accumulation patterns by sex and ethnicity using international datasets. An amalgamated and cross-calibrated dataset of dual x-ray absorptiometry (DXA)-measured variables compiled segmental mass for bone mineral content (BMC), lean mass (LM), and fat mass (FM) for each participant; percentage of segment fat (PSF) was calculated as PSFsegment = (FMsegment/(BMCsegment + LMsegment + FMsegment)) × 100. A total of 30 587 adults (N = 16 490 females) from 13 datasets were included. A regression model was used to examine differences in regional fat mass and PSF. All populations followed the same segmental fat mass accumulation in the ascending order with statistical significance (arms < legs < trunk), except for Hispanic/Latinx males (arms < [legs = trunk]). Relative fat accumulation patterns differed between those with greater PSF in the appendages (Arab, Mexican, Asian, Black, American Caucasian, European Caucasian, and Australasian Caucasian females; Black males) and those with greater PSF in the trunk (Mexican, Asian, American Caucasian, European Caucasian, and Australasian Caucasian males). Greater absolute and relative fat accumulation in the trunk could place males of most ethnicities in this study at a higher risk of visceral fat deposition and associated co-morbidities.

Associations of Serum Uric Acid to High-Density Lipoprotein Cholesterol Ratio with Trunk Fat Mass and Visceral Fat Accumulation.

It has been reported recently that the ratio of uric acid to high-density lipoprotein cholesterol (UHR) is correlated with several metabolic disorders. The present study aimed to investigate the associations of UHR with body fat content and distribution. This study enrolled 300 participants (58 men and 242 women) aged 18 to 65 years. The levels of serum uric acid and high-density lipoprotein cholesterol were measured by standard enzymatic methods. The overall fat content and segmental fat distribution were assessed with an automatic bioelectrical impedance analyzer. In the population with obesity, the visceral fat area (VFA) and subcutaneous fat area (SFA) were measured using magnetic resonance imaging. Among the study population, 219 individuals (73.0%) were with obesity. The median level of UHR in individuals with obesity was 33.7% (26.2% - 45.9%), which was significantly higher than that in those without obesity [22.6% (17.0% - 34.4%), P < 0.01]. UHR was positively associated with overall fat content and segmental fat distribution parameters (all P < 0.01). In multivariate linear regression analysis, compared with body mass index, waist circumference was more closely associated with UHR (standardized β = 0.427, P < 0.001) after adjusting for confounding factors. Additionally, total fat mass (standardized β = 0.225, P = 0.002) and trunk fat mass (standardized β = 0.296, P = 0.036) were more closely linked to UHR than total fat-free mass and leg fat mass, respectively. In the population with obesity, VFA was independently correlated with UHR (P < 0.01), while SFA was not associated with UHR. UHR was significantly associated with overall fat content and trunk fat accumulation. In the population with obesity, UHR was positively associated with VFA. Attention should be paid to the role of excessive trunk fat mass in the relationship between UHR and metabolic disorders.

New hopes on "SLU-PP-332" as an effective agent for weight loss with indirect kidney protection efficacy; a nephrology point of view

SLU-PP-332 activates estrogen receptor-related orphan receptors, increasing energy expenditure, fatty acid oxidation, and decreasing fat mass accumulation. The drug enhances mitochondrial function and cellular respiration in skeletal muscle cell lines, increases the expression of an estrogen receptor-related orphan receptor target gene, and enhances mitochondrial respiration in C2C12 myocytes. The drug also increases oxidative fibers in skeletal muscle and improves exercise endurance in C57BL/6J mice.

Three different oils improve HFD‐induced lipid metabolism disorders via driving gut microbiota

AbstractSchizochytrium sp. L. oil (SO), fish oil (FO), and sacha inchi oil (SIO) can regulate high‐fat diet‐induced obesity, but the effect on gut microbiota and the mechanism remain unclear. This study aimed to find out the different effects of the three oils mediated the gut microbiota on lipid metabolism. In comparison with the high‐fat diet (HFD) group, SO, FO, and SIO could reduce fat mass accumulation and decrease the levels of the serum and liver biochemical parameters in mice. The regulatory effect on gut microbiota in mice is determined by 16S rRNA gene high‐throughput sequencing. Caulobacter, Acetatifactor, and Mucispirillum as dominant bacterial genus are enriched in intervention groups. SO, SIO, and FO could distinctly decrease interleukin 6, nuclear factor‐kappa B, tumor necrosis factor‐alpha, sterol regulatory element‐binding protein 1c, FAS, and HMGCR expressions in liver, upregulate the expression of acyl‐coenzyme A oxidase 1 and A acetyltransferases and regulate the thermogenesis. SO, SIO, and FO has a comprehensive impact on lipid metabolism by the expression of genes related to fat synthesis, cholesterol synthesis, inflammation, energy consumption, the structure of intestinal flora, abundance of beneficial bacteria, and intestinal diversity. Based on these results, SO, SIO, and FO may be used as functional food to drive beneficial changes in gut microbiota and then regulate the lipid metabolism disorders.Practical Applications: Obesity‐related diseases caused by lipid metabolism disorders have driven the rapid development of the diet drug market. However, the side effects of diet drugs on the human body also make the majority of consumers worried. Natural oil products that regulate lipid metabolism disorders and dietary obesity provide a substitute. Schizochytrium sp. L. oil (SO), fish oil (FO), and sacha inchi oil (SIO) are rich in high‐quality unsaturated fatty acids and are not suitable for high temperature cooking but can be eaten in low temperature cooking and sauces and so on. SO, FO, and SIO can be used to develop functional food that could reduce lipid metabolism disorders.

Gut microbiota in overweight and obesity: crosstalk with adipose tissue.

Overweight and obesity are characterized by excessive fat mass accumulation produced when energy intake exceeds energy expenditure. One plausible way to control energy expenditure is to modulate thermogenic pathways in white adipose tissue (WAT) and/or brown adipose tissue (BAT). Among the different environmental factors capable of influencing host metabolism and energy balance, the gut microbiota is now considered a key player. Following pioneering studies showing that mice lacking gut microbes (that is, germ-free mice) or depleted of their gut microbiota (that is, using antibiotics) developed less adipose tissue, numerous studies have investigated the complex interactions existing between gut bacteria, some of their membrane components (that is, lipopolysaccharides), and their metabolites (that is, short-chain fatty acids, endocannabinoids, bile acids, aryl hydrocarbon receptor ligands and tryptophan derivatives) as well as their contribution to the browning and/or beiging of WAT and changes in BAT activity. In this Review, we discuss the general physiology of both WAT and BAT. Subsequently, we introduce how gut bacteria and different microbiota-derived metabolites, their receptors and signalling pathways can regulate the development of adipose tissue and its metabolic capacities. Finally, we describe the key challenges in moving from bench to bedside by presenting specific key examples.

Glucocorticoid Receptor Antagonism Improves Glucose Metabolism in a Mouse Model of Polycystic Ovary Syndrome.

Polycystic ovary syndrome (PCOS) is a complex metabolic disorder associated with obesity, insulin resistance, and dyslipidemia. Hyperandrogenism is a major characteristic of PCOS. Increased androgen exposure is believed to deregulate metabolic processes in various tissues as part of the PCOS pathogenesis, predominantly through the androgen receptor (AR). Notably, various metabolic features in PCOS are similar to those observed after excess glucocorticoid exposure. We hypothesized that glucocorticoid receptor (GR) signaling is involved in the metabolic symptoms of PCOS. In a PCOS model of chronic dihydrotestosterone (DHT) exposure in female mice, we investigated whether GR signaling machinery was (de)regulated, and if treatment with a selective GR antagonist alleviated the metabolic symptoms. We observed an upregulation of GR messenger RNA expression in the liver after DHT exposure. In white adipose tissues and liver we found that DHT upregulated Hsd11b1, which encodes for the enzyme that converts inactive into active glucocorticoids. We found that preventive but not therapeutic administration of a GR antagonist alleviated DHT-induced hyperglycemia and restored glucose tolerance. We did not observe strong effects of GR antagonism in DHT-exposed mice on other features like total fat mass and lipid accumulation in various tissues. We conclude that GR activation may play a role in glucose metabolism in DHT-exposed mice.

Differences in muscle mass and fat mass accumulation in youth female athletes

Differences in muscle mass and fat mass accumulation in youth female athletes

Adolescent food insecurity in female rodents and susceptibility to diet-induced obesity

Food insecurity is defined as having limited or uncertain access to nutritious foods, and adolescent food insecurity is associated with obesity and disordered eating behaviors in humans. We developed a rodent model of adolescent food insecurity to determine whether adolescent food insecurity per se promotes increased susceptibility to diet-induced obesity and altered eating behaviors during adulthood. Female juvenile Wistar rats were singly housed and assigned to three experimental diets: food-secure with standard chow (CHOW), food-secure with a high-fat/sugar Western diet (WD), and food-insecure with WD (WD-FI). Food-secure rats (CHOW and WD) received meals at fixed feeding times (9:00, 13:00, and 16:00). WD-FI rats received meals at unpredictable intervals of the above-mentioned feeding times but had isocaloric amounts of food to WD. We investigated the impact of adolescent food insecurity on motivation for sucrose (Progressive Ratio), approach-avoidance behavior for palatable high-fat food (Approach-Avoidance task), and susceptibility to weight gain and hyperphagia when given an obesogenic choice diet. Secondary outcomes were the effects of food insecurity during development on anxiety-like behaviors (Open Field and Elevated Plus Maze) and learning and memory function (Novel Location Recognition task). Rodents with adolescent food insecurity showed a greater trend of weight gain and significantly increased fat mass and liver fat accumulation on an obesogenic diet in adulthood, despite no increases in motivation for sucrose or high-fat food. These data suggest that adolescent unpredictable food access increases susceptibility to diet-induced fat gain without impacting food motivation or food intake in female rodents. These findings are among a small group of recent studies modeling food insecurity in rodents and suggest that adolescent food insecurity in females may have long-term implications for metabolic physiology later in life.

О взаимосвязи некоторых антропометрических индексов с биоимпедансной оценкой относительной жировой массы у детей и подростков

Introduction. The study of adiposity in children and adolescents is an important issue in the era of the global epidemic of obesity. Body mass index is the most common, but not the only body fat index. There are also indexes based on waist and hip circumferences. The purpose of this work is to analyze the age variability and correlation between various anthropometric indices and bioimpedance estimates of the percentage of body fat in children and adolescents. Materials and methods. We analyzed the data of children and adolescents of both sexes 7-17 years old, 1885 boys and 1453 girls, collected in the course of cross-sectional anthropological surveys of schoolchildren in Moscow, Arkhangelsk and the Arkhangelsk region. Body mass index (BMI), waist-to-hip ratio (WHR), waist-to-height ratio (WHtR), hip-to-height ratio (HHtR) were calculated. The percentage of fat mass (% FM) was obtained by bioimpedance with the ABC-01 “Medas” device. Correlation analysis was used to assess the relationship between indices and %FM. Results and discussion. The paper analyzes the age-related variability of height and weight, BMI, waist circumference, hip circumference, WHR, WHtR, HHtR and % FM in children and adolescents of both sexes. Age-related changes in % FM have clear sex differences. In girls, during puberty, there is an accumulation of fat mass, while in boys – its decrease. Body weight, BMI, waist circumference, hip circumference, HHtR increase in the process of growth, WHR and WHtR decrease. For all indicators, except for WHR, in boys and girls in younger age groups, correlations with % FM are high and decrease with age, reaching average values. While the correlations of WHR with %FM are weak in all studied age groups. Conclusion. Based on the analysis performed, it is shown that body mass, waist circumference, hip circumference, BMI, WHtR, HHtR are good predictors of relative body fat mass, they significantly correlate with % FM, while WHR correlates very weakly. @ 2023. This work is licensed under a CC BY 4.0 license

The role of mitochondria in the pathogenesis of sarcopenia: a concise review

The aging process results in progressive loss of muscle mass and strength, a condition known as sarcopenia. At biological-molecular level, this condition is characterized by numerous changes that occur in the muscle cell, such as increased protein degradation, apoptosis, altered autophagy process, impaired myogenic pathway, and mitochondrial dysfunction. The purpose of this concise review is to provide a brief overview of the involvement of mitochondria in the pathogenesis of sarcopenia, highlighting the potential involvement of carnitine palmitoyl transferase 1, an enzyme localized in the outer mitochondrial membrane, involved in the transport of long-chain fatty acids into the mitochondrion for β-oxidation. This protein is a potential new player in the pathogenesis of sarcopenia, since it may be responsible for the accumulation of fat mass and the development of insulin resistance in the muscle tissue of affected subjects, thus suggesting a new pathway underlying the onset and progression of the disease. KEY WORDS: Sarcopenia, mitochondria, muscle, mitochondrial dysfunction, energy metabolism.