Fat Tissue Weight Research Articles

Integration of Lipidomics and Transcriptomics Identifies the Regulation of Lipid Homeostasis as Potential Mechanisms of Konjac Glucomannan against Hepatic Steatosis.

Hepatic steatosis is characterized by substantial disruption in the liver's lipid level regulation. Konjac glucomannan (KGM) is acknowledged as a nutritious food that has the potential to prevent hyperlipidemia. This study utilized lipidomics and transcriptomics to investigate the efficacy of KGM in alleviating high-fat diet-induced hepatic steatosis by regulating lipid homeostasis. The findings indicated that supplementation of KGM for a duration of 10 weeks led to significant decreases in body weight, liver weight, and epididymal fat tissue weight. Furthermore, improvements in lipid concentrations in plasma and liver samples were observed, along with enhancements in glucose tolerance and the mitigation of liver damage. Additionally, lipidomics analysis revealed that the primary differential lipid metabolites were mainly associated with fatty acid metabolism pathways. Transcriptomic analysis showed that KGM significantly altered the gene expression of the peroxisome proliferator-activated receptor (PPAR) signaling pathway in the liver. Moreover, KGM demonstrated a significant regulatory impact on the hepatic expression of PPARγ, potentially mitigating hepatic steatosis through modulation of the PPARγ-mediated lipid metabolism pathway. In conclusion, these findings suggest that KGM effectively mitigates steatosis by modulating hepatic lipid metabolites and controlling PPARγ-mediated genes in the liver.

Tlr9 deficiency in B cells leads to obesity by promoting inflammation and gut dysbiosis

Toll-like receptor 9 (TLR9) recognizes bacterial, viral and self DNA and play an important role in immunity and inflammation. However, the role of TLR9 in obesity is less well-studied. Here, we generate B-cell-specific Tlr9-deficient (Tlr9fl/fl/Cd19Cre+/-, KO) B6 mice and model obesity using a high-fat diet. Compared with control mice, B-cell-specific-Tlr9-deficient mice exhibited increased fat tissue inflammation, weight gain, and impaired glucose and insulin tolerance. Furthermore, the frequencies of IL-10-producing-B cells and marginal zone B cells were reduced, and those of follicular and germinal center B cells were increased. This was associated with increased frequencies of IFNγ-producing-T cells and increased follicular helper cells. In addition, gut microbiota from the KO mice induced a pro-inflammatory state leading to immunological and metabolic dysregulation when transferred to germ-free mice. Using 16 S rRNA gene sequencing, we identify altered gut microbial communities including reduced Lachnospiraceae, which may play a role in altered metabolism in KO mice. We identify an important network involving Tlr9, Irf4 and Il-10 interconnecting metabolic homeostasis, with the function of B and T cells, and gut microbiota in obesity.

Ginseng polysaccharide components attenuate obesity and liver lipid accumulation by regulating fecal microbiota and hepatic lysine degradation

The increasing incidence of obesity has led to widespread attention in the exploration of natural ingredients. Ginseng polysaccharides (PGP), the main components from Panax ginseng, have been reported potential effect to attenuate obesity and regulate lipid metabolism. In this study, we found that PGP inhibited the high-fat diet (HFD)-induced weight gain, fat ratio and fat tissue weight after 8-week administration. Serum and liver lipid analysis showed that PGP decreased the levels of triglyceride and total cholesterol, which was mediated by the inhibition of key genes for fatty acid and cholesterol metabolisms. Metabolomics studies showed that the inhibitory effect of PGP on liver lipid accumulation was significantly correlated with its regulation of citric acid cycle and lysine degradation. PGP regulated the expression of genes related to lysine degradation in both liver tissue and hepatocytes. In addition, PGP reshaped the composition of fecal microbiota at the genus and species levels in obese mice. Spearman's correlation analysis demonstrated that Staphylococcus sciuri, Staphylococcus lentus, and Pseudoflavonifractor sp. An85 may be the potential targets that PGP maintains the abundance of l-lysine against obesity. It concluded that PGP can attenuate obesity and liver lipid accumulation by regulating fecal microbiota and hepatic lysine degradation.

Anti-obesity effects of a standardized ethanol extract of Eisenia bicyclis by regulating the AMPK signaling pathway in 3T3-L1 cells and HFD-induced mice.

Obesity requires treatment to mitigate the potential development of further metabolic disorders, including diabetes, hyperlipidemia, tumor growth, and non-alcoholic fatty liver disease. We investigated the anti-obesity effect of a 30% ethanol extract of Eisenia bicyclis (Kjellman) Setchell (EEB) on 3T3-L1 preadipocytes and high-fat diet (HFD)-induced obese C57BL/6 mice. Adipogenesis transcription factors including peroxisome proliferator-activated receptor (PPAR)γ, CCAAT/enhancer-binding protein-alpha (C/EBPα), and sterol regulatory element-binding protein-1 (SREBP-1) were ameliorated through the AMP-activated protein kinase (AMPK) pathway by EEB treatment in differentiated 3T3-L1 cells. EEB attenuated mitotic clonal expansion by upregulating cyclin-dependent kinase inhibitors (CDKIs) while downregulating cyclins and CDKs. In HFD-fed mice, EEB significantly decreased the total body weight, fat tissue weight, and fat in the tissue. The protein expression of PPARγ, C/EBPα, and SREBP-1 was increased in the subcutaneous fat and liver tissues, while EEB decreased the expression levels of these transcription factors. EEB also inhibited lipogenesis by downregulating acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS) expression in the subcutaneous fat and liver tissues. Moreover, the phosphorylation of AMPK and ACC was downregulated in the HFD-induced mouse group, whereas the administration of EEB improved AMPK and ACC phosphorylation; thus, EEB treatment may be related to the AMPK pathway. Histological analysis showed that EEB reduced the adipocyte size and fat accumulation in subcutaneous fat and liver tissues, respectively. EEB promotes thermogenesis in brown adipose tissue and improves insulin and leptin levels and blood lipid profiles. Our results suggest that EEB could be used as a potential agent to prevent obesity.

Litter reduction-induced obesity promotes early depressive-like behavior and elevated prefrontal cortex GFAP expression in male offspring

AimsThe present study was developed to investigate how litter reduction-induced obesity promotes early depressive-related behaviors in rodent offspring. Main methodsWe employed a standardized litter size reduction protocol, dividing litters into groups: normal litters (NL), consisting of six males and six females pups and small litters (SL), comprising two males and two females pups. Maternal behavior was monitored during the initial week of lactation. Subsequently, we assessed the pups for weight gain, locomotor activity, social play behavior, and performance in forced swimming test. We further evaluated the weights of retroperitoneal and perigonadal fat tissues, along with the expression of glial fibrillary acidic pprotein (GFAP) in the hippocampus and prefrontal cortex of the offspring. Key findingsOur results indicated that litter size reduction led to an increased the maternal behavior. In contrast, offspring from the SL group displayed greater weight gain and increased, retroperitoneal and perigonadal fat. Both male and female rodents in the SL group exhibited decreased social play behavior, and male offspring spent more time immobile during the forced swimming test, suggesting a depressive-like phenotype. Notably, we observed an increase in the GFAP expression in the prefrontal cortex of male rodents, with a trend toward increased expression in the hippocampus. SignificanceObesity may facilitate the development of early depressive-like behaviors, potentially associated with elevated GFAP expression in the prefrontal cortex.

Korean fermented soybean paste (Doenjang) has anti-obesity and anti-hypertensive effects via the renin-angiotensin system (RAS) in high-fat diet-induced obese rats.

The health-beneficial outcomes of doenjang, a Korean fermented food have been questioned due to its high salt content; moreover, the detailed underlying mechanisms of its health beneficial effects are not fully investigated. Thus, this study aimed to investigate doenjang's anti-obesity effects, anti-hypertensive effects, and its underlying mechanisms in high-fat diet -induced obesity. Sprague-Dawley rats fed with normal diet (ND), high-fat diet (HD), HD with 8% additive salt (HDS), or HD with doenjang containing 8% salt (HDJ) for 13 weeks. Compared to HD and HDS groups, the HDJ group had lower body and epididymal fat tissue weight gain and showed hypotrophy and hypoplasia. The RAS-related mRNA levels in the adipose tissue, including Renin and Ace were downregulated in the HDJ group compared to HD and HDS groups. Additionally, HDJ groups had significant improvements in systolic blood pressure, serum RAS-associated parameters (e.g., angiotensin II and aldosterone), renal mRNA levels related to RAS (e.g., angiotensin II receptor type 1 and 2), and aldosterone-associated mRNA expressions (e.g., mineralocorticoid receptor) in the kidney of HD-induced obese rats. Most importantly, HDS and HDJ groups showed distinct outcomes regarding adipogenesis and electrolytes metabolism, even though both diets contain a high level of salt. HDS group showed a higher epididymal fat tissue weight, mass, and adipocyte size than HDJ group. In addition, compared with HDJ group, HDS group significantly decreased the release of Na+ and K+ throughout the urine and feces. The present study addresses that doenjang has anti-obesity effects and anti-hypertensive effects by activating RAS in the adipose tissue and kidney, respectively. Additionally, this study also demonstrates that salt in doenjang and the additive salt differently influences adipogenesis and electrolytes metabolism, supporting doenjang has health advantageous effects regardless of its high salt contents.

Olvanil inhibits adipocyte differentiation in 3T3-L1 cells, reduces fat accumulation and improves lipidic profile on mice with diet-induced obesity

AimThe present study is aimed to examine olvanil's effect in preadipocyte cell culture and on a murine model of diet-induced obesity. We hypothesized that olvanil by being a capsaicinoid will reduce the differentiation to mature adipocytes and reduce the weight of fat tissue in the studied mice. MethodsTo determine the effect of olvanil on adipogenesis, 3T3-L1 cells were cultured. Oil red staining was performed to determine lipid accumulation, whereas triglycerides were measured by biochemical determination. Expression of PPAR-γ and PREF-1 were measured by RT-PCR. Therefore, male C57BL/6J mice (CICUAL:2018-020B) were fed with a high-fat diet for 12 weeks to develop a murine model of diet-induced obesity (DIO). Animals were separated into 6 experimental groups: control (standard diet), DIO (high-fat diet), DIO + orlistat (10 mg/kg), DIO + olvanil (10 mg/kg), DIO + olvanil (25 mg/kg) and DIO + olvanil (50 mg/kg), olvanil was administered for 4 weeks. ResultsOlvanil inhibits adipogenesis, reduces lipid accumulation and triglycerides in 3T3-L1 adipocytes. PPAR-ɣ gene expression was suppressed while PREF-1 was increased in adipocytes treated with olvanil. Whereas protein expression of FABP4 and PPAR-ɣ decreases significantly with olvanil. The results suggest that olvanil can inhibit the differentiation of preadipocytes to adipocytes through the overexpression or maintenance of PREF-1 levels and the suppression of PPAR-ɣ, and FABP4. Therefore, in diet-induced obesity in mice, olvanil decreases fat accumulation in the body and improve lipid profile by decreasing LDL, VLDL and triglycerides in serum. ConclusionOlvanil inhibits adipocyte differentiation in 3T3-L1 cells and reduces fat accumulation and ameliorate lipid profile in diet-induced obese mice.

High-protein compound yogurt with quinoa improved clinical features and metabolism of high-fat diet–induced nonalcoholic fatty liver disease in mice

Gut microbiota dysbiosis plays a crucial role in the occurrence and progression of nonalcoholic fatty liver disease (NAFLD), which may be influenced by nutritional supplementation. Quinoa, a type of pseudocereal, has gained prominence due to its high nutritional value and diverse applications. This study aimed to determine whether yogurt containing quinoa can ameliorate NAFLD and alleviate metabolic disorders by protecting against the divergence of gut microbiota. Our findings suggested that quinoa yogurt could significantly reduce the body weight gain and fat tissue weight of high-fat diet (HFD)-fed obese mice. In addition, quinoa yogurt significantly reduced liver steatosis and enhanced glucose homeostasis and insulin sensitivity. Additional research indicates that quinoa yogurt can reduce the levels of proinflammatory cytokines (i.e., tumor necrosis factor α, IL-1β, and IL-6) and inhibit endotoxemia and systemic inflammation. The characteristics of the gut microbiota were then determined by analyzing 16S rRNA. In addition, we discovered that the gut microbiota was disturbed by HFD consumption. Particularly, intestinal probiotics and beneficial intestinal secretions were increased, leading to the expression of glucagon-like peptide-1 in the colon, contributing to NAFLD. Furthermore, endotoxemia and systemic inflammation in HFD-fed mice were restored to the level of control mice when they were fed yogurt and quinoa. Therefore, yogurt containing quinoa can effectively alleviate NAFLD symptoms and may exert its effects via microbiome-gut-liver axis mechanisms. According to some research, the role of the enteric-liver axis may also influence metabolic disorders to reduce the development of NAFLD.

Anti-Obesity Effects of SPY Fermented with Lactobacillus rhamnosus BST-L.601 via Suppression of Adipogenesis and Lipogenesis in High-Fat Diet-Induced Obese Mice.

In this research, the potential anti-obesity efficacy of Lactobacillus rhamnosus BST-L.601 and its fermented product (named SPY) with mashed sweet potato paste were investigated using 3T3-L1 preadipocytes and high-fat diet (HD)-induced obese mice. SPY (0-0.5 mg/mL) dose-dependently and significantly reduced lipid accumulation and TG content and the expression of adipogenic markers (C/EBPα, PPAR-γ, and aP2) and fatty acid synthetic pathway proteins (ACC and FAS) in 3T3-L1 adipocytes, demonstrating that SPY suppresses adipocyte differentiation and lipogenesis. Oral administration of SPY (4 × 107 CFU/kg body weight) to HD-induced obese mice for 12 weeks significantly reduced the body and liver weight, the size of adipocytes, and the weight of epididymal, visceral, and subcutaneous fat tissues. SPY was more effective in decreasing body weight gain in HD mice than in treatment with BST-L.601 alone. Administration of SPY or BST-L.601 also reduced the serum level of total cholesterol and LDL cholesterol and leptin secretion at a similar level. These results revealed that both SPY and BST-L.601 effectively suppress HD-induced adipogenesis and lipogenesis, suggesting that these materials would be useful in the functional foods industry to ameliorate and/or prevent obesity.

Effects of Turmeric Extract on Age-Related Skeletal Muscle Atrophy in Senescence-Accelerated Mice.

Muscle atrophy is one of the main causes of sarcopenia-the age-related loss of skeletal muscle. In this study, we investigated the effect of turmeric (Curcuma longa) extract (TE) supplementation on age-related muscle atrophy in a senescence-accelerated mouse model and explored the underlying mechanisms. Twenty-six-week-old male, senescence-accelerated mouse resistant (SAMR) mice received the AIN-93G basal diet, while twenty-six-week-old male, senescence-accelerated mouse prone 8 (SAMP8) mice received the AIN-93G basal diet or a 2% TE powder-supplemented diet for ten weeks. Our findings revealed that TE supplementation showed certain effects on ameliorating the decrease in body weight, tibialis anterior weight, and mesenteric fat tissue weight in SAMP8 mice. TE improved gene expression in the glucocorticoid receptor-FoxO signaling pathway in skeletal muscle, including redd1, klf15, foxo1, murf1, and mafbx. Furthermore, TE might have the certain potential on improving the dynamic balance between anabolic and catabolic processes by inhibiting the binding of glucocorticoid receptor or FoxO1 to the glucocorticoid response element or FoxO-binding element in the MuRF1 promoter in skeletal muscle, thereby promoting muscle mass and strength, and preventing muscle atrophy and sarcopenia prevention. Moreover, TE may have reduced mitochondrial damage and maintained cell growth and division by downregulating the mRNA expression of the genes mfn2 and tsc2. Thus, the results indicated TE's potential for preventing age-related muscle atrophy and sarcopenia.

Carcass characteristics and meat quality of lambs fed diets with different roughage: concentrate ratios supplemented with liquid residue of cassava

The objective of this study was to evaluate the effects of lambs fed two roughage: concentrate (R:C) ratios, with or without the liquid residue of cassava (LRC) on carcass traits and meat quantity. Forty lambs (19.5 ± 1.45 kg body weight), non-castrated, crossbred Santa Inês were distributed in a completely randomized 2 × 2 factorial design. There was no effect (p > 0.05) of the inclusion of LRC on the variables. The roughage:concentrate ratio of 40:60 promoted higher values for empty body weight, hot carcass weight, cold carcass weight, subcutaneous thickness fat, cooling loss, Longissimus muscle area, carcass morphometric measurements, and commercial cuts. Higher weight of leg, muscles, fat, bone and other tissues, as well as for the ratio muscle:fat, and muscle:bone was observed in lambs fed 40R:60C. For the meat chemical composition, there was the effect (p < 0.05) only for ether extract (EE) for lambs fed 40R:60C ratio. The redness (a*) of meat was greater (p < 0.05) for lambs fed 80R:20C. The other physicochemical characteristics were not influenced. The roughage:concentrate ratio of 40:60 improves the carcass traits and commercial cuts, but does not promote changes in meat quality, independent of supplementation with liquid residue of cassava.

Pachyrhizus erosus Inhibits Adipogenesis via the Leptin-PPARγ-FAS Pathway in a High-Fat Diet-Induced Mouse Model

In 2016, obese patients represented 13% of the worldwide adult population, and by 2030, they are projected to make up 34%. Obesity is an incommunicable disease, but it can induce many health problems. The groups consisted of a control, a 65% high-fat group, and a 250 mg/kg P. erosus group. Several biomarkers, such as body weight gain, the presence of TC/LDL/HDL in the serum, the weight of fat tissue, and liver weight/morphology, were investigated to define the anti-obesity mechanisms of P. erosus, and the adipogenesis pathway was studied. P. erosus suppressed body weight gain, decreased TC and LDL, prevented fat tissue weight gain, and prevented liver weight gain by blocking lipid droplet accumulation. P. erosus effectively decreased the up-regulated levels of leptin, significantly controlled both C/EBPα and PPARγ levels, and prevented increased FAS expression levels. We concluded that P. erosus effectively controlled obesity by regulating leptin-C/EBPα-PPARγ and FAS and might be a promising AOM.

Assessment of the Impact of Physical Activity on the Musculoskeletal System in Early Degenerative Knee Joint Lesions in an Animal Model.

Osteoarthritis (OA) is one of the most prevalent diseases of the osteoarticular system. Progressive destruction of joints is accompanied by development of pathological changes in the muscle tissue, i.e., weakening, atrophy, and remodelling (sarcopenia). The aim of the present study is to assess the impact of physical activity on the musculoskeletal system in an animal model of early degenerative lesions in the knee joint. The study involved 30 male Wistar rats. The animals were allocated to three subgroups of 10 animals each. Each animal from the three subgroups received sodium iodoacetate by injection into the patellar ligament of the right knee joint, whereas saline was administered through the patellar ligament in the left knee joint. The rats in the first group were stimulated to exercise on a treadmill. The animals in the second group were allowed to lead a natural lifestyle (no treadmill stimulation). In the third group, all parts of the right hind limb muscle were injected with Clostridium botulinum toxin type A. The study demonstrated that, compared to the active rats, bone density in the immobilised rats decreased, as indicated by the densitometric assessment of the whole body and the examination of rats' hind limbs and knee joints alone. This clearly evidenced the impact of physical activity on bone mineralisation. The weight of both fat and muscle tissues in the physically inactive rats was reduced. Additionally, the adipose tissue had higher weight in the entire right hind limbs, where monoiodoacetic acid was administered to the knee joint. The animal model clearly showed the importance of physical activity in the early stages of OA, as it slows down the process of joint destruction, bone atrophy, and muscle wasting, whereas physical inactivity contributes to progression of generalised changes in the musculoskeletal system.

Sesamin Attenuates Obesity-Associated Nonalcoholic Steatohepatitis in High-Fat and High-Fructose Diet-Fed Mice.

This study explored the effects of sesamin on nonalcoholic steatohepatitis (NASH). High-fat and high-fructose diet-fed mice supplemented with or without sesamin. The results suggested that sesamin-treated mice lost body weight and fat tissue weight, had lower levels of serum metabolic parameters, and insulin resistance was mitigated. Histological examinations showed that sesamin treatment mitigated the progression of hepatic steatosis, and inflammation. In addition, sesamin enhanced hepatic antioxidant capacity, and decreased the activations of hepatic c-jun N-terminal kinase, inhibitor of kappa B kinase α, and insulin receptor substrate 1 as well as hepatic interleukin-6 and tumor necrosis factor-alpha levels. Further experiments indicated that sesamin treatment downregulated GRP78 and phospho-inositol-requiring enzyme 1 (IRE1) expression, and upregulated x-box binding protein 1 (XBP1) expression in hepatic tissue. The aforementioned results suggest that sesamin alleviates obesity-associated NASH, which might be linked to the effect of sesamin on the regulation of the hepatic endoplasmic reticulum stress-IRE1/XBP1 pathway. Thus, sesamin may be a good food functional ingredient in the treatment of obesity-associated NASH.

Organic vegetable juice supplement alleviates hyperlipidemia in diet-induced obese mice and modulates microbial community in continuous colon simulation system.

In this study, we investigated the effects of organic vegetable juice (OVJ) supplementation on modulating the microbial community, and how its consumption ameliorated blood-lipid profiles in diet-induced obese mice. Here, we studied the alleviating effect of hyperlipidemia via animal experiments using diet-induced obese mice and analyzed the effect of OVJ on the microbial community in continuous colon simulation system. OVJ consumption did not have a significant effect on weight loss but helped reduce the weight of the epididymis fat tissue and adipocytes. Additionally, blood-lipid profiles, such as triglyceride, high-density lipoprotein, and glucose, were improved in the OVJ-fed group. Expression levels of genes related to lipid synthesis, including SREBP-1, PPARγ, C/EBPα, and FAS, were significantly decreased. In addition, OVJ treatment significantly reduced inflammatory cytokines and oxidative stress. OVJ supplement influenced intestinal bacterial composition from phylum to genus level, including decreased Proteobacteria in the ascending colon in the phylum. At the family level, Akkermansia, which are associated with obesity, were significantly augmented in the transverse colon and descending colon compared to the control juice group. In addition, treatment with OVJ affected predicted lipid-metabolism-function genes related to lipid synthesis. These results suggest that OVJ supplementation may modulate gut microbial community and reduce the potential symptom of hyperlipidemia in diet-obese mice.

D-Limonene Promotes Anti-Obesity in 3T3-L1 Adipocytes and High-Calorie Diet-Induced Obese Rats by Activating the AMPK Signaling Pathway.

D-limonene (LIM) is a common monoterpene compound, principally found in citrus essential oils. This study investigated the anti-obesity effect of LIM on the 5′-adenosine monophosphate (AMP)-activated protein kinase (AMPK) signaling pathway in 3T3-L1 adipocytes and high-calorie diet-induced obese rats and confirmed the optimally effective dose of LIM. The 3T3-L1 adipocytes were treated with 0.05−0.4 mg/mL LIM for 10 days and oil red O and triglyceride (TG) content were used to determine the levels of lipid accumulation. The results showed that more than 0.05 mg/mL LIM inhibited lipid accumulation by reducing oil red O in 3T3-L1 adipocytes. Masses of 0.2 and 0.4 mg/mL LIM also decreased the TG contents in 3T3-L1 adipocytes. On the other hand, Wistar rats were given high-calorie diets, combined with LLIM (154 mg/kg) and HLIM (1000 mg/kg) treatments, for 16 weeks. The result shows that LLIM and HLIM decreased body weight, total fat tissue weight, and serum low-density lipoprotein-cholesterol (LDLc) levels. HLIM reduced serum TG and increased serum lipase and high-density lipoprotein-cholesterol (HDLc) levels. Moreover, the anti-obesity metabolic pathway showed that LIM (>0.05 mg/mL) in 3T3-L1 adipocytes and LIM (>154 mg/kg) in high-calorie diet-induced obese rats could activate the AMPK signaling pathway. The activated AMPK regulated the mRNA expression related to adipogenesis (PPARγ, C/EBPα, FABP4), lipogenesis (SREBP-1c, ACC, FAS), and lipolysis (ATGL, HSL) to inhibit obesity. This finding demonstrates that LIM has anti-obesity properties. Namely, it is seen that LIM acts by regulating the AMPK signaling pathway in 3T3-L1 adipocytes and high-calorie diet-induced obese rats. In terms of dose−response, LIM (154 mg/kg) would be an optimal effective dose for anti-obesity induced by a high-calorie diet.

The Effect of Calorie Restriction on Body Weight, Fat Tissue Weight and the Histopathological Picture of Fat Tissue in Rats

Background : Calorie restriction is a reduction in calorie intake without malnutrition, as the main tool to improve health (Tomiyama et al.,2017). Limitation of calorie intake around 20-40% of total calorie intake, but intake remains adequate to reduce inflammation (Trepanowski et al., 2010). Obesity is one of the consequences of excessive calorie consumption which causes inflammation so that it can increase the risk of degenerative diseases (Susantiningsih, 2015). Overweight is divided into two, namely hypertrophy occurs by the accumulation of large amounts of fat in unilocular fat cells, so that the size of fat cells reaches four times larger, but the number of fat cells does not increase. And hyperplasia is a heavy obesity because in addition to growing cells also the number of cells becomes more (Sunny Wangko, 2014). One effort that can be done to reduce the increase in degenerative diseases is by limiting caloric intake or appropriate calorie restriction (Brzek et al., 2012).Purpose : This study purpose to determine changes in body weight, fat tissue and histopathological features of fat tissue in rats given calorie restriction and reviewed according to Islamic views.Methods : This type of research is an experimental laboratory for 6 weeks with research subjects male white rats (Wistar Strain) which is divided into 2 groups, namely control, and Calorie Restrictions Taking samples of body weight and fat tissue in the abdomen and supraclavicular to see the number of cells fat, fat cell size and weight of white fat tissue and brown fat tissue.Results : Calorie restriction can reduce fat cell size, and weight of white fat tissue significantly (p <0.05). in brown fat there was a significant increase. but in the measurement of body weight and fat cell numbers there were no significant differences (p> 0.05).Conclusion : In calorie restriction there was no significant relationship after a study of body weight and fat cell count, but found a significant relationship to the weight of white fat tissue and brown fat tissue and the size of fat cells. In Islamic view calorie restriction is the same as limiting food intake as recommended by the Prophet about 1/3 of the stomach for food.

Methanolic fruit extract of Myrica nagi protects the hypothalamus and attenuates inflammation associated with gold thioglucose- and high-fat diet-induced obesity via various adipokines

BackgroundMyrica nagi is popular in unani and ayurveda. Chemical constituents like myricetin isolated from its fruit has been shown to exert beneficial effects against cardiovascular disease, cancer, inflammatory conditions, and metabolic disorders. ObjectivesThis study aimed to elucidate the anti-obesity effect of the methanolic extract of M. nagi (MEMN) using in vivo animal models of obesity induced by gold thioglucose or a high-fat diet. Materials and methodsThe obese mice were treated or untreated with MEMN for 8 weeks. Thereafter, feed intake, Lee index, and body mass index (BMI); biochemical parameters such as lipid profile, liver enzymes and specific biomarkers of obesity, including insulin, leptin, adiponectin, free fatty acids (FFA), monocyte chemoattractant protein (MCP)-1, and resistin, were recorded. The weight and histopathology of organs and fat tissue were examined to validate the effectiveness of the extract. ResultsMEMN administration at various doses significantly reduced the induced weight gain, feed intake, BMI, and Lee index. Adipose tissue decreased as the MEMN dose increased. MEMN attenuated liver enzyme activity, decreased lipid, leptin, MCP-1, resistin, and FFA levels, and increased adiponectin levels. It also increased protection of liver cells and decreased accumulation of mesenteric fat. ConclusionsMEMN supplementation decreased weight and improved obesity serum/plasma lipid biomarker, insulin, leptin, adiponectin, MCP-1, and resistin levels. The weight-reducing activity of MEMN may be mediated by decreased gastrointestinal fat absorption and modulation of inflammation associated signaling pathways, leading to reduced adipose inflammation associated with energy expenditure.

Eggshell membrane modulates gut microbiota to prevent murine pre-cachexia through suppression of T helper cell differentiation.

BackgroundCachexia is a life‐threatening condition observed in several pathologies, such as cancer or chronic diseases. Interleukin 10 (Il10) gene transfer is known to improve cachexia by downregulating Il6. Here, we used an IL10‐knockout mouse model to simulate cachexia and investigate the effects of eggshell membrane (ESM), a resistant protein, on general pre‐cachexia symptoms, which is particularly important for the development of cachexia therapeutics.MethodsFive‐week‐old male C57BL6/J mice were fed an AIN‐93G powdered diet (WT), and 5‐week‐old male B6.129P2‐Il10 < tm1Cgn>/J (IL10−/−) mice were fed either the AIN‐93G diet (KO) or an 8% ESM‐containing diet (KOE) for 28 weeks. The tissue weight and levels of anaemia‐, blood glucose‐, lipid metabolism‐, and muscular and colonic inflammation‐related biochemical markers were measured. Transcriptomic analysis on liver and colon mucus and proteomic analysis on skeletal muscle were performed. Ingenuity Pathway Analysis was used to identify molecular pathways and networks. Caecal short‐chain fatty acids (SCFAs) were identified using HPLC, and caecal bacteria DNA were subjected to metagenomic analysis. Flow cytometry analysis was performed to measure the CD4+ IL17+ T cells in mesenteric lymph nodes.ResultsThe body weight, weight of gastrocnemius muscle and fat tissues, colon weight/length ratio, plasma HDL and NEFA, muscular PECAM‐1 levels (P < 0.01), plasma glucose and colonic mucosal myeloperoxidase activity (P < 0.05) and T helper (Th) 17 cell abundance (P = 0.071) were improved in KOE mice over KO mice. Proteomic analysis indicated the protective role of ESM in muscle weakness and maintenance of muscle formation (>1.5‐fold). Transcriptomic analysis revealed that ESM supplementation suppressed the LPS/IL1‐mediated inhibition of RXR function pathway in the liver and downregulated the colonic mucosal expression of chemokines and Th cell differentiation‐related markers (P < 0.01) by suppressing the upstream BATF pathway. Analysis of the intestinal microenvironment revealed that ESM supplementation ameliorated the microbial alpha diversity and the abundance of microbiota associated with the degree of inflammation (P < 0.05) and increased the level of total organic acids, particularly of SCFAs such as butyrate (2.3‐fold), which could inhibit Th1 and Th17 production.ConclusionsESM supplementation ameliorated the chief symptoms of cachexia, including anorexia, lean fat tissue mass, skeletal muscle wasting and reduced physical function. ESM also improved colon and skeletal muscle inflammation, lipid metabolism and microbial dysbiosis. These results along with the suppressed differentiation of Th cells could be associated with the beneficial intestinal microenvironment and, subsequently, attenuation of pre‐cachexia. Our findings provide insights into the potential of ESM in complementary interventions for pre‐cachexia prevention.

Mogroside-Rich Extract From Siraitia grosvenorii Fruits Ameliorates High-Fat Diet-Induced Obesity Associated With the Modulation of Gut Microbiota in Mice.

Siraitia grosvenorii is a kind of medicinal food plant. The mogroside-rich extract (MGE) of its fruits can effectively ameliorate obesity, but the underlying mechanisms remain underexplored. In this study, we aimed to determine whether MGE can ameliorate obesity by protecting against the divergences of gut microbiota. Mice were challenged with a high-fat diet (HFD) and treated with MGE by oral gavage. Then, the characteristics of the gut microbiota were determined by 16S rDNA analysis. Our findings showed that MGE could significantly reduce body weight gain and fat tissue weight of the mice fed with HFD. Moreover, MGE markedly attenuated fatty liver, and improved glucose tolerance and insulin sensitivity. We further found that the gut microbiota structures were disturbed by HFD feeding. In particular, the abundance of Firmicutes was increased and the abundance of Bacteroidetes was decreased, resulting in an increased proportion of Firmicutes to Bacteroidetes (F/B), which contributes to obesity. Interestingly, the abnormal proportion of F/B of HFD feeding mice was restored to the level of control mice by MGE treatment. Additionally, the abundances of obesogenic microbiota, such as Ruminiclostridium and Oscillibacter were also decreased after MGE treatment. In summary, our findings demonstrate that MGE can modulate gut microbiota in obese mice and shed new light on how it alleviates obesity.