Increased Adipose Tissue Mass Research Articles

Sex-Specific Effects of Maternal and Post-Weaning High-Fat Diet on Adipose Tissue Remodeling and Asprosin Expression in Mice Offspring.

Perinatal high-fat diet (HFD) increases risk of metabolic disorders in offspring. Adipose tissue remodeling is associated with metabolic syndrome. The current study characterizes the profile of maternal HFD-induced changes in adipose tissue remodeling and adipokines expression in mice offspring. Female C57BL/6 mice are fed with CHOW or HFD for 2 weeks before mating, throughout gestation and lactation. At weaning, pups are randomly fed with CHOW or HFD, resulting in eight groups according to sex and maternal diet: Male CHOW-CHOW (MCC), Male CHOW-HFD (MCH), Male HFD-CHOW (MHC), Male HFD-HFD (MHH), Female CHOW-CHOW (FCC), Female CHOW-HFD (FCH), Female HFD-CHOW (FHC), and Female HFD-HFD (FHH). Increased body weight, impaired glucose tolerance, increased adipose tissue mass and hypertrophy, and decreased circulating asprosin level are only observed in male offspring exposure to maternal HFD. Serum asprosin level negatively correlates with fasting blood glucose, serum cholesterol (CHO), and high-density lipoprotein (HDL) levels, while positively correlates with serum low-density lipoprotein (LDL) and glutamate-oxaloacetate transaminase (GOT) levels in male offspring. A combination of genetic and biochemical analyses of adipokines shows the depot- and sex-specific changes in response to maternal and/or post-weaning HFD. This study's results reveal the differential metabolic changes in response to maternal and/or post-weaning HFD in male and female offspring. The effect of maternal HFD on metabolic phonotype is more obvious in male offspring, supporting the notion that males are more susceptible to HFD-induced metabolic disorders.

Activation of the adipocyte CREB/CRTC pathway in obesity

Obesity is a major risk factor for the development of type II diabetes. Increases in adipose tissue mass trigger insulin resistance via the release of pro-inflammatory cytokines from adipocytes and macrophages. CREB and the CRTC coactivators have been found to promote insulin resistance in obesity, although the mechanism is unclear. Here we show that high fat diet feeding activates the CREB/CRTC pathway in adipocytes by decreasing the expression of SIK2, a Ser/Thr kinase that phosphorylates and inhibits CRTCs. SIK2 levels are regulated by the adipogenic factor C/EBPα, whose expression is reduced in obesity. Exposure to PPARγ agonist rescues C/EBPα expression and restores SIK2 levels. CRTC2/3 promote insulin resistance via induction of the chemokines CXCL1/2. Knockout of CRTC2/3 in adipocytes reduces CXCL1/2 expression and improves insulin sensitivity. As administration of CXCL1/2 reverses salutary effects of CRTC2/3 depletion, our results demonstrate the importance of the CREB/CRTC pathway in modulating adipose tissue function.

Analysis of the trophic status of patients with coronavirus disease complicated by cavernous sinus thrombosis

It is known that Covid-19 disease is severe in obese and elderly people. The study once again proves the high risk of complications in these patients. Identification of risk factors based on an assessment of the trophic status of patients complicated by cavernous sinus thrombosis. In the multidisciplinary clinic of the Tashkent Medical Academy, in 36 patients with Postcovid syndrome complicated by thrombosis of the cavernous sinus. The average age of the patients was 60 ± 8 years, of which 26 women (57.8%) and 19 men (42.2%). All patients underwent an bioimpedancometry (Tanita BS-585, Japan). Deviations from the ideal body weight were found in 87% of cases, body weight deficiency was noted in 14% of patients, an increase in adipose tissue mass in 73% of patients. The average values of the indicator of total and visceral fat mass were 23% higher than their characteristic physiological norm, lack of muscle mass from 13 to 25 kg was revealed. The total percentage of water in the body varied from 35 to 65%, since in overweight patients below normal - 42.2 ± 2.12 (p ≤ 0.01). The calculated indicator of basal metabolism on average corresponded to 1995.1 ± 50.34 kcal, which is 18% lower than the required value, but indicates a reduced physical activity. According to bioimpedancemetric analyzes, the deviation of many indicators of the composition components of the body was interpreted, as it means a violation of the physical, metabolic status. Such patients have a high risk of complications, unfavorable outcome of the underlying disease.

Single or combined ablation of peripheral serotonin and p21 limit adipose tissue expansion and metabolic alterations in early adulthood in mice fed a normocaloric diet.

Identifying the fundamental molecular factors that drive weight gain even in the absence of hypercaloric food intake, is crucial to enable development of novel treatments for the global pandemic of obesity. Here we investigated both adipose tissue-specific and systemic events that underlie the physiological weight gain occurring during early adulthood in mice fed a normocaloric diet. In addition, we used three different genetic models to identify molecular factors that promote physiological weight gain during normocaloric and hypercaloric diets. We demonstrated that normal physiological weight gain was accompanied by an increase in adipose tissue mass and the presence of cellular and metabolic signatures typically found during obesity, including adipocyte hypertrophy, macrophage recruitment into visceral fat and perturbed glucose metabolism. At the molecular level, this was associated with an increase in adipose tissue tryptophan hydroxylase 1 (Tph1) transcripts, the key enzyme responsible for the synthesis of peripheral serotonin. Genetic inactivation of Tph1 was sufficient to limit adipose tissue expansion and associated metabolic alterations. Mechanistically, we discovered that Tph1 inactivation resulted in down-regulation of cyclin-dependent kinase inhibitor p21Waf1/Cip1 expression. Single or double ablation of Tph1 and p21 were equally effective in preventing adipocyte expansion and systemic perturbation of glucose metabolism, upon both normocaloric and hypercaloric diets. Our results suggest that serotonin and p21 act as a central molecular determinant of weight gain and associated metabolic alterations, and highlights the potential of targeting these molecules as a pharmacologic approach to prevent the development of obesity.

Growth Hormone Receptor Gene Disruption in Mature-Adult Mice Improves Glucose Metabolism and Lifespan in Females

Growth hormone (GH) serves an important role in early and adult life. Reduction of GH action has been shown to increase life span in many species of animals. In fact, mice bearing a congenital disruption of GH receptor (GHR) gene (GHRKO) hold the record for the longest-lived laboratory mice. In addition to extended life span, these mice show improved health with lower rates of cancer, increased insulin sensitivity, and resistance to age-associated cognitive decline. Furthermore, humans with decreased GH action due to inactivating mutations in the GHR (Laron Syndrome patients) are resistant to cancer and diabetes. Even though the beneficial effects of congenital Ghr gene disruption are well studied, the consequences of postnatal disruption of GH action were unknown. Previously our laboratory generated a mouse line with disrupted GH action at 1.5 months of age (1.5mGHRKO mice). Results showed that these mice had improved insulin sensitivity and increased maximal lifespan only in females, yet growth retardation was still present.To consider decreased GH action as a possible therapeutic to extend healthy lifespan, it was imperative to elucidate the effects of disrupting Ghr gene at a mature-adult age, well after the developmental and growth period of the mice. To this end, we hypothesized that removal of GH action in adult life would convey some of the same health and life span benefits seen in the GHRKO mice without the reduced body length. To test this hypothesis, we used the cre-lox system to generate mice with a disrupted Ghr gene at a mature-adult age (6 months), referred as 6mGHRKO mice. We then performed a phenotypic and lifespan characterization, and tested for molecular mechanisms known to be associated with extended longevity, namely oxidative stress resistance and mTOR modulation. We found that similar to GHRKO and 1.5mGHRKO mice, disruption of GHR at 6 months of age resulted in mice with increased adipose tissue mass, decreased lean mass, high circulating GH, but decreased insulin growth factor-1 levels compared to control mice. Furthermore, the 6mGHRKO mice displayed significantly improved insulin sensitivity in males, with no changes in glucose tolerance. Also, serum levels of inflammatory markers and liver triglycerides were unchanged in these mice. Experiments to evaluate the status of oxidative damage and mTOR activation in liver, skeletal muscle and subcutaneous adipose tissue of male and female 6mGHRKO mice showed a tissue-specificity and sexual dimorphism in these results. Importantly, male and female 6mGHRKO mice showed no change in body length, but mean, median and maximal lifespan were significantly extended in females. In conclusion, disruption of GH action well past sexual maturation produces beneficial effects on insulin sensitivity and aging in mice. Acknowledgements: This work is supported by the State of Ohio’s Eminent Scholar Program, by NIH grant AG059779 and by the AMVETS.

Cytotoxicity and Antiobesity Activity of Freeze-Dried Malus domestica, Canarium sp. and Averrhoa bilimbi Fruit

Obesity has a role in the development of diseases such as diabetes, cardiovascular disease and hyperlipidemia which is characterized by the increase of adipose tissue mass due to an imbalance of energy intake and expenditure. Freeze-dried fruits are well known to possess antiobesity activity. In this study, we have evaluated the antiobesity activity of freeze-dried fruit (M. domestica, Canarium sp., and A. bilimbi) using CHOL, G6PDH, TG level, and Oil Red O assay. The viability of 3T3-L1 cell in the Canarium sp. freeze-dried in the concentration of 12.50 µg/ml has a higher value compared to M. domestica and A. bilimbi. The measurements of CHOL, G6PDH, TG level, and Oil Red O assay of the M. domestica freeze-dried in the concentration of 75 μg/ml has higher inhibitory activity compared to the Canarium sp. and A. bilimbi freeze-dried. In the CHOL assay, M. domestica freeze-dried has a higher value compared to A. bilimbi and Canarium sp. In the G6PDH assay, the freeze-dried of M. domestica has the value of 49.56%, Canarium sp. (45.22%), and A. bilimbi (47.13%), while in the Oil Red O assay, M. domestica has inhibition activity of 62.63%, A. bilimbi 50.01% and Canarium sp. 44.13%. The level of TG showed that M. domestica has higher activity with the value of 60.61%, A. bilimbi 57.54%, while Canarium sp. 55.03%. The freeze-dried of M. domestica in the concentration of 75 μg/ml has good inhibitory activity of lipid compared to A. bilimbi and Canarium sp.

GPR10 gene deletion in mice increases basal neuronal activity, disturbs insulin sensitivity and alters lipid homeostasis.

G-protein-coupled receptor GPR10 is expressed in brain areas regulating energy metabolism. In this study, the effects of GPR10 gene deficiency on energy homeostasis in mice of both sexes fed either standard chow or a high-fat diet (HFD) were studied, with a focus on neuronal activation of PrRP neurons, and adipose tissue and liver metabolism. GPR10 deficiency in males upregulated the phasic and tonic activity of PrRP neurons in the nucleus of the solitary tract. GPR10 knockout (KO) males on a standard diet displayed a higher body weight than their wild-type (WT) littermates due to an increase in adipose tissue mass; however, HFD feeding did not cause weight differences between genotypes. Expression of lipogenesis genes was suppressed in the subcutaneous adipose tissue of GPR10 KO males. In contrast, GPR10 KO females did not differ in body weight from their WT controls, but showed elevated expression of lipid metabolism genes in the liver and subcutaneous adipose tissue compared to WT controls. An attenuated non-esterified fatty acids change after glucose load compared to WT controls suggested a defect in insulin-mediated suppression of lipolysis in GPR10 KO females. Indirect calorimetry did not reveal any differences in energy expenditure among groups. In conclusion, deletion of GPR10 gene resulted in changes in lipid metabolism in mice of both sexes, however in different extent. An increase in adipose tissue mass observed in only GPR10 KO males may have been prevented in GPR10 KO females owing to a compensatory increase in the expression of metabolic genes.

Epigenetic Regulation of Adipogenesis in Development of Metabolic Syndrome.

Obesity is one of the biggest public health concerns identified by an increase in adipose tissue mass as a result of adipocyte hypertrophy and hyperplasia. Pertaining to the importance of adipose tissue in various biological processes, any alteration in its function results in impaired metabolic health. In this review, we discuss how adipose tissue maintains the metabolic health through secretion of various adipokines and inflammatory mediators and how its dysfunction leads to the development of severe metabolic disorders and influences cancer progression. Impairment in the adipocyte function occurs due to individuals’ genetics and/or environmental factor(s) that largely affect the epigenetic profile leading to altered gene expression and onset of obesity in adults. Moreover, several crucial aspects of adipose biology, including the regulation of different transcription factors, are controlled by epigenetic events. Therefore, understanding the intricacies of adipogenesis is crucial for recognizing its relevance in underlying disease conditions and identifying the therapeutic interventions for obesity and metabolic syndrome.

A Transcriptomic Analysis Reveals Novel Patterns of Gene Expression During 3T3-L1 Adipocyte Differentiation.

BackgroundObesity is characterized by increased adipose tissue mass that results from increased fat cell size (hypertrophy) and number (hyperplasia). The molecular mechanisms that govern the regulation and differentiation of adipocytes play a critical role for better understanding of the pathological mechanism of obesity. However, the mechanism of adipocyte differentiation is still unclear.ObjectiveThe present study aims to compare the gene expression changes during adipocyte differentiation in the transcriptomic level, which may help to better understand the mechanism of adipocyte differentiation.MethodsRNA sequencing (RNA-seq) technology, GO and KEGG analysis, quantitative RT-PCR, and oil red O staining methods were used in this study.ResultsA lot of genes were up- or down-regulated between each two differentiation stages of 3T3-L1 cells. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed that lipid metabolism and oxidation–reduction reaction were mainly involved in the whole process of adipocyte differentiation. Decreased immune response and cell cycle adhesion occurred in the late phase of adipocyte differentiation, which was demonstrated by divergent expression pattern analysis. Moreover, quantitative RT-PCR results showed that the mRNA expression levels of Trpv4, Trpm4, Trpm5, and Trpm7 were significantly decreased in the differentiated adipocytes. On the other hand, the mRNA expression levels of Trpv1, Trpv2, Trpv6, and Trpc1 were significantly increased in the differentiated adipocytes. Besides, the mRNA expressions of TRPV2 and TRPM7 were also significantly increased in subcutaneous white adipose tissue from diet-induced mice. In addition, the activation of TRPM7, TRPV1, and TRPV2 suppressed the differentiation of adipocytes.ConclusionThese data present the description of transcription profile changes during adipocyte differentiation and provides an in-depth analysis of the possible mechanisms of adipocyte differentiation. These data offer new insight into the understanding of the mechanisms of adipocyte differentiation.

DILTIAZEM PREVENTS MONOSODIUM GLUTAMATE TOXICITY IN THE RAT TESTES

Increased exposure to food additives may exhibit harmful effect on the male reproductive system. Neonatal application of high doses of popular taste enhancer monosodium glutamate (MSG) to different kinds of animals cause lesions of the hypothalamic nuclei and the retina. Later in adulthood, animals exhibit a series of neuroendocrine disorders (stunted growth, obesity and decreased fertility). The mechanism of MSG action is not completely explained yet. We hypothesized that high concentration of MSG could alter permeability of neural membrane for calcium. The objective of our study was to find out whether the pretreatment with diltiazem, a calcium channel blocker, could prevent harmful effect of MSG in the rat testes. Male rat pups were treated with: 0.9% sodium chloride (C group), 4 mg/g BW of MSG (M group), 5 mg/g BW of diltiazem (D group) and diltiazem 5 mg/g BW with MSG (DM group) on 2nd , 4th , 6th , 8th, 10th postnatal day. Animals were sacrificed at the age of six months. MSG treatment resulted in: stunted growth (decreased naso-anal length and tail length; p < 0.05), decreased relative testis weight (p < 0.05), and increased adipose tissue mass (Lee index; p < 0.05), testicular atrophy and decreased histomorphometric parameters (tubular area, tubular perimeter, Feret diameter, tubular diameter, epithelial height; p < 0.001). The rats of C, D and DM groups had normal testicular histology and morphometric parameters. Pretreatment with diltiazem has prevented the development of morphological disorders of testes. Our results suggest that calcium overloading may play an important role among mechanisms of MSG testicular toxicity.

Evaluation of Fat Accumulation and Adipokine Production during the Long-Term Adipogenic Differentiation of Porcine Intramuscular Preadipocytes and Study of the Influence of Immunobiotics.

The degree of fat accumulation and adipokine production are two major indicators of obesity that are correlated with increased adipose tissue mass and chronic inflammatory responses. Adipocytes have been considered effector cells for the inflammatory responses due to their capacity to express Toll-like receptors (TLRs). In this study, we evaluated the degree of fat accumulation and adipokine production in porcine intramuscular preadipocyte (PIP) cells maintained for in vitro differentiation over a long period without or with stimulation of either TNF-α or TLR2-, TLR3-, or TLR4-ligands. The cytosolic fat accumulation was measured by liquid chromatography and the expression of adipokines (CCL2, IL-6, IL-8 and IL-10) were quantified by RT-qPCR and ELISA at several time points (0 to 20 days) of PIP cells differentiation. Long-term adipogenic differentiation (LTAD) induced a progressive fat accumulation in the adipocytes over time. Activation of TLR3 and TLR4 resulted in an increased rate of fat accumulation into the adipocytes over the LTAD. The production of CCL2, IL-8 and IL-6 were significantly increased in unstimulated adipocytes during the LTAD, while IL-10 expression remained stable over the studied period. An increasing trend of adiponectin and leptin production was also observed during the LTAD. On the other hand, the stimulation of adipocytes with TLRs agonists or TNF-α resulted in an increasing trend of CCL2, IL-6 and IL-8 production while IL-10 remained stable in all four treatments during the LTAD. We also examined the influences of several immunoregulatory probiotic strains (immunobiotics) on the modulation of the fat accumulation and adipokine production using supernatants of immunobiotic-treated intestinal immune cells and the LTAD of PIP cells. Immunobiotics have shown a strain-specific ability to modulate the fat accumulation and adipokine production, and differentiation of adipocytes. Here, we expanded the utility and potential application of our in vitro PIP cells model by evaluating an LTAD period (20 days) in order to elucidate further insights of chronic inflammatory pathobiology of adipocytes associated with obesity as well as to explore the prospects of immunomodulatory intervention for obesity such as immunobiotics.

Human Thymic Involution and Aging in Humanized Mice.

Thymic involution is an important factor leading to the aging of the immune system. Most of what we know regarding thymic aging comes from mouse models, and the nature of the thymic aging process in humans remains largely unexplored due to the lack of a model system that permits longitudinal studies of human thymic involution. In this study, we sought to explore the potential to examine human thymic involution in humanized mice, constructed by transplantation of fetal human thymus and CD34+ hematopoietic stem/progenitor cells into immunodeficient mice. In these humanized mice, the human thymic graft first underwent acute recoverable involution caused presumably by transplantation stress, followed by an age-related chronic form of involution. Although both the early recoverable and later age-related thymic involution were associated with a decrease in thymic epithelial cells and recent thymic emigrants, only the latter was associated with an increase in adipose tissue mass in the thymus. Furthermore, human thymic grafts showed a dramatic reduction in FOXN1 and AIRE expression by 10 weeks post-transplantation. This study indicates that human thymus retains its intrinsic mechanisms of aging and susceptibility to stress-induced involution when transplanted into immunodeficient mice, offering a potentially useful in vivo model to study human thymic involution and to test therapeutic interventions.

Bioimpedance analysis in determining body composition in women with systemic lupus erythematosus: a pilot study

Objective: to determine body composition (BC) in women with systemic lupus erythematosus (SLE), by using bioimpedance analysis.Patients and methods. The investigation enrolled 12 women with a reliable diagnosis of SLE, who were followed up at the Clinic of the V.A. Nasonova Research Institute of Rheumatology. Their median age was 46.5 [38.5; 54.7] years. All the patients underwent estimation of waist circumference (WC) and body mass index (BMI). BC was analyzed using an InBody 770 multi-frequency bioimpedance analyzer (Biospace Co. Ltd, South Korea) at the Clinical Nutrition Clinic, Federal Research Institute of Nutrition and Biotechnology.Results and discussion. BMI corresponding to overweight or obesity was observed in 67% of patients; abdominal obesity (AO) was seen in 83%. BC study showed that in most patients, adipose tissue mass was greater than the normal values (75%), lean body mass, skeletal muscle mass, and the amount of body water were within normal limits (83%), and the basal metabolic rate was reduced (67%). There were positive correlations between the percentage of adipose tissue and BMI (r=0.9; p&lt;0.01), WC (r=0.7; p&lt;0.01), C-reactive protein (CRP) levels (r=0.6; p&lt;0.05), and complement C3 concentrations (r=0.9; p&lt;0.01). Similar results were obtained when assessing the relationship between visceral fat area and BMI (r=0.9; p&lt;0.01), WC (r=0.78; p&lt;0.01), CRP (r=0.6; p&lt;0.05), complement component C3 (r=0.8; p&lt;0.01). There was an inverse correlation between visceral fat area and the Systemic Lupus Erythematosus Disease Activity Index 2000 (SLEDAI-2K) (r=-0.6; p&lt;0.05).Conclusion. Most women with SLE have AO, increased adipose tissue mass, normal lean body mass, and decreased basal metabolism. There is a direct correlation of visceral fat content and inflammatory markers (CRP, complement component C3) and an inverse correlation of those with the SLEDAI-2K.

Impaired glucose transport in inguinal adipocytes after short-term high-sucrose feeding in mice

Diets enriched in sucrose severely impair metabolic regulation and are associated with obesity, insulin resistance and glucose intolerance. In the current study, we investigated the effect of 4 weeks high-sucrose diet (HSD) feeding in C57BL6/J mice, with specific focus on adipocyte function. Mice fed HSD had slightly increased adipose tissue mass but displayed similar hepatic triglycerides, glucose and insulin levels, and glucose clearance capacity as chow-fed mice. Interestingly, we found adipose depot-specific differences, where both the non- and insulin-stimulated glucose transports were markedly impaired in primary adipocytes isolated from the inguinal fat depot from HSD-fed mice. This was accompanied by decreased protein levels of both GLUT4 and AS160. A similar but much less pronounced trend was observed in the retroperitoneal depot. In contrast, both GLUT4 expression and insulin-stimulated glucose uptake were preserved in adipocytes isolated from epididymal adipose tissue with HSD. Further, we found a slight shift in cell size distribution towards larger cells with HSD and a significant decrease of ACC and PGC-1α expression in the inguinal adipose tissue depot. Moreover, fructose alone was sufficient to decrease GLUT4 expression in cultured, mature adipocytes.Altogether, we demonstrate that short-term HSD feeding has deleterious impact on insulin response and glucose transport in the inguinal adipose tissue depot, specifically. These changes occur before the onset of systemic glucose dysmetabolism and therefore could provide a mechanistic link to overall impaired energy metabolism reported after prolonged HSD feeding, alone or in combination with HFD.

Effects of different dietary vegetable oils on growth and intestinal performance, lipid metabolism and flesh quality in gilthead sea bream

This study tests the effects of feeding different vegetable oils (VO) in gilthead sea bream with the aim of improving sustainable aquafeeds. Juveniles were fed ad libitum with ten isonitrogenous (46%) and isolipidic (22%) diets with a 75% fish oil (FO) replacement, differing in VO composition leading to two experimental blocks: fish fed with VO blends or mono-substituted diets. Growth parameters, skin and muscle colour, muscle texture, plasma metabolites, digestive capacities, and transcript levels of intestinal lipid transport, muscle dynamics and lipid metabolism-related genes in white muscle and adipose tissue were studied. In fish fed high-palm oil diets, final body weight and mesenteric fat significantly increased, while effects were not found in hepatosomatic index, reflecting tissue-specific lipid accumulation. Relative intestinal length increased significantly with dietary soya oil (SO) content, suggesting a compensatory mechanism to improve nutrient absorption capacity. Plasma parameters showed few changes upon dietary treatments. Lipase activity was unaltered, while intestinal fatp1b expression increased in animals fed blended diets high in rapeseed oil (RO). In adipose tissue, expression of nuclear receptors pparβ and lxr was modified by dietary fatty acids (FA) profile; however, regarding lipid metabolism and β-oxidation genes, only lpl showed significant differences, suggesting that FA uptake and oxidation, but not de novo lipogenesis is what appears to determine the increase in adipose tissue mass. In fish fed blended VO diets, lpl expression showed a positive correlation with MUFA dietary content, suggesting that some FA present in RO enhance its expression, according to data from fish fed mono-substituted diets. In muscle, fish fed blended VO diets also showed a positive correlation of lpl expression with dietary MUFA, whereas in mono-substituted, it was significantly higher in fish fed SO, suggesting other mechanisms are involved in LPL regulation. Concerning β-oxidation genes in muscle, significant differences were detected in cpt1a expression for fish fed blended VO diets, whereas hadh and cpt1b were unaltered, suggesting slight FA uptake regulation in mitochondria. Expression levels of genes related to myogenic processes were not greatly modified by dietary lipid sources except for myogenin in blended VO diets-fed fish, showing a similar profile as that in body weight and opposite with the differentiation marker mhc. This study provides new information regarding the effects of dietary VO, demonstrating moderate effects in lipid homeostasis without adverse effects on growth performance, leading to a transversal view of the responses and interactions from intestine to muscle growth and flesh quality.

Anti-obesity effects of dichloromethane leaf extract of Gnidia glauca in high fat diet-induced obese rats

BackgroundObesity is a chronic metabolic disorder characterized by increased adipose tissue mass due to positive energy balance. Prescription of anti-obesity drugs can be useful adjuncts to diet and exercise for obese patients who have failed to achieve weight loss. However, these drugs are ineffective and are associated with adverse effects. In recent times, medicinal plants have drawn a sharp focus owing to their biocompatibility and effectiveness. Attempts to determine the therapeutic effects and identification of bio-active principles from herbal prescriptions have become the prime focus in the validation of their folkloric usage and in drug discovery programs. Therefore, the present study aimed to determine the anti-obesity effects of Dichloromethane leaf extract of Gnidia glauca in high-fat-diet-induced obese rats. MethodsObesity was induced experimentally in white albino Wistar rats by feeding them with prepared high-fat-diet and water ad libitum for a period of 12 weeks. The in-vivo anti-obesity effects were determined by oral administration of Gnidia glauca at dosage levels of 200, 250 and 300 mg/kg body weight from the 6th to 12th week of study. Phytochemical analysis of Gnidia glauca was conducted using gas chromatography linked to mass spectrophotometer. ResultsThe results indicated that Gnidia glauca exhibited potent anti-obesity effects. It significantly reduced the body weight, organ weights, organo-somatic indices, anthropometric indices, the total fat content, adiposity index, atherogenic index as well as various lipid profiles. It also decreased the total feed intake. However, it significantly increased levels of high-density lipoproteins and rectal body temperature of rats. Quantitative phytochemical analysis also revealed the presence of various phytocompounds that have shown to be associated with anti-obesity effects. ConclusionThe anti-obesity effects of Gnidia glauca maybe attributed to the phytochemicals present. The present study, therefore, scientifically validates the traditional use of Gnidia glauca as a potential candidate for the synthesis of new effective anti-obesity supplement.

A new perspective of lactatogenesis by isolated adipocytes

Increased adipose tissue mass exhibited greater capacity of glucose transformation in lactate, highlighting lactatogenesis as a crucial factor in body size. Classically, lactate produced by isolated adipocytes are expressed per million of cells and were never correlated with their size. Spontaneously hypertensive rats (SHR) have a lower body weight and smaller adipocytes when compared to Wistar-Kyoto. We evaluated basal lactate by epididymal 15-weeks-old isolated adipocytes of SHR, Wistar-Kyoto and Wistar. Basal lactate was similar when expressed by one million cells. However, SHR adipocytes were smaller, so we adjusted the results by cell volume and SHR showed higher basal lactate production which was directly endorsed by hyperlactatemia in the presented conditions. Thereby, we suggest a new perspective on lactatogenesis analysis by adipocytes, which could be linked to the receptors density and associate enzymes. Moreover, we showed that the thin and hypertensive rats can be hyperlactemic in fasting conditions.

Protective effect of Betula utilis bark extract on high fat diet induced obesity in Wistar rats

BackgroundThe metabolic complications due to increased incidence of obesity, is now recognized as a major public health problem. In current era herbal medicine has been recognised as adjuvant therapy for the treatment of several clinical implications. ObjectivesThe current investigation is aimed to explore the anti-obesity effects pertaining to Betula utilis (BU) ethanolic extract in high-fat diet (HFD) induced obesity and hyperlipidemic rat model. MethodsExperimental obesity was developed in the male rats by administering HFD for 10 weeks. Initial and final body weight, Lee index, Body mass index (BMI), fat pads weight, serum glucose, triglyceride (TG), total cholesterol (TC) and various lipoproteins were estimated in the current study. ResultsAfter four week of HFD treatment, BU (100–400 mg/kg/day p.o) was given along with high fat diet for further 6 weeks which significantly reduced HFD induced body weight gain and increase in adipose tissue mass in a dose dependant manner. Moreover, BU attenuated HFD induced augmented serum glucose, TG and TC. The anti-obesity potential of BU was comparable to a well established marketed drug orlistat. ConclusionThese results reflect that BU supplementation decreases body weight, improves obesity serum biomarkers (TG, TC, LDL), and the weight reducing activity of BU may be mediated by decreased fat absorption from the GIT.

Immune-Deficient Pfp/Rag2−/− Mice Featured Higher Adipose Tissue Mass and Liver Lipid Accumulation with Growing Age than Wildtype C57BL/6N Mice

Aging is a risk factor for adipose tissue dysfunction, which is associated with inflammatory innate immune mechanisms. Since the adipose tissue/liver axis contributes to hepatosteatosis, we sought to determine age-related adipose tissue dysfunction in the context of the activation of the innate immune system fostering fatty liver phenotypes. Using wildtype and immune-deficient mice, we compared visceral adipose tissue and liver mass as well as hepatic lipid storage in young (ca. 14 weeks) and adult (ca. 30 weeks) mice. Adipocyte size was determined as an indicator of adipocyte function and liver steatosis was quantified by hepatic lipid content. Further, lipid storage was investigated under normal and steatosis-inducing culture conditions in isolated hepatocytes. The physiological age-related increase in body weight was associated with a disproportionate increase in adipose tissue mass in immune-deficient mice, which coincided with higher triglyceride storage in the liver. Lipid storage was similar in isolated hepatocytes from wildtype and immune-deficient mice under normal culture conditions but was significantly higher in immune-deficient than in wildtype hepatocytes under steatosis-inducing culture conditions. Immune-deficient mice also displayed increased inflammatory, adipogenic, and lipogenic markers in serum and adipose tissue. Thus, the age-related increase in body weight coincided with an increase in adipose tissue mass and hepatic steatosis. In association with a (pro-)inflammatory milieu, aging thus promotes hepatosteatosis, especially in immune-deficient mice.

Sex Difference in Corticosterone-Induced Insulin Resistance in Mice.

Prolonged exposure to glucocorticoids (GCs) causes various metabolic derangements. These include obesity and insulin resistance, as inhibiting glucose utilization in adipose tissues is a major function of GCs. Although adipose tissue distribution and glucose homeostasis are sex-dependently regulated, it has not been evaluated whether GCs affect glucose metabolism and adipose tissue functions in a sex-dependent manner. In this study, high-dose corticosterone (rodent GC) treatment in C57BL/6J mice resulted in nonfasting hyperglycemia in male mice only, whereas both sexes displayed hyperinsulinemia with normal fasting glucose levels, indicative of insulin resistance. Metabolic testing using stable isotope-labeled glucose techniques revealed a sex-specific corticosterone-driven glucose intolerance. Corticosterone treatment increased adipose tissue mass in both sexes, which was reflected by elevated serum leptin levels. However, female mice showed more metabolically protective adaptations of adipose tissues than did male mice, demonstrated by higher serum total and high-molecular-weight adiponectin levels, more hyperplastic morphological changes, and a stronger increase in mRNA expression of adipogenic differentiation markers. Subsequently, in vitro studies in 3T3-L1 (white) and T37i (brown) adipocytes suggest that the increased leptin and adiponectin levels were mainly driven by the elevated insulin levels. In summary, this study demonstrates that GC-induced insulin resistance is more severe in male mice than in female mice, which can be partially explained by a sex-dependent adaptation of adipose tissues.