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Obstructive sleep apnea-hypopnea syndrome (OSAHS) is characterized by repeated oxygen desaturation. Obesity and visceral fat accumulation (VFA) are risk factors for the development of OSAHS. Circulating leptin increases in accordance with body mass index (BMI), and under experimental conditions intermittent hypoxia stimulates leptin production The primary objective of this study was to investigate whether hypoxemia during sleep influences the levels of circulating leptin and whether the location of body fat deposits, ie, the distribution of VFA and subcutaneous fat accumulation (SFA), affects circulating leptin levels in patients with OSAHA who are not obese. We assessed VFA and SFA by abdominal CT scan and measured circulating levels of leptin in 96 male patients with OSAHS and 52 male patients without OSAHS matched for BMI. To be matched for BMI in the two groups, patients whose BMIs were < 27 were selected for the OSAHS group In the whole study group, circulating leptin levels correlated with BMI (r = 0.30), VFA (r = 0.44), SFA (r = 0.28), apnea-hypopnea index (AHI) [r = 0.48], sleep mean arterial oxygen saturation (Sao2) [r = 0.59], and sleep lowest Sao2 (r = 0.37). Multiple regression analysis showed that average Sao2 (p < 0.01) and lowest Sao2 (p = 0.03) were explanatory variables for serum leptin values, but AHI (p = 0.054), BMI (p = 0.33), VFA (p = 0.11), and SFA (p = 0.36) were not These results suggest that sleep hypoxemia may be the main determinant of circulating leptin levels, although the location of body fat deposits could contribute to the elevated circulating leptin levels in patients with OSAHS who are not obese

•Sodium short-chain fatty acids regulated metabolic status mainly or partly by reduced feed intake.•Sodium short-chain fatty acids attenuated fat deposition via regulating related genes and hormones.•Sodium short-chain fatty acids could modulate mitochondrial function and beige adipogenesis. Acetate, propionate, and butyrate, three of the most common short-chain fatty acids (SCFAs), can be produced when some non-digestible carbohydrates enter the large intestine and undergo bacterial fermentation. The aim of this study was to investigate the effects of these three SCFAs on appetite regulation and lipid metabolism and to determine the extent that appetite contributes to the beneficial influences of SCFAs. In a 35-d study, 48 C57BL/6J male mice were randomly allocated to six groups: control; 5% sodium acetate; 5% sodium propionate; 5% sodium butyrate; pair fed 1; and pair fed 2. The study showed that dietary supplementation of sodium acetate reduced serum triacylglycerol, free fatty acids, glucose, and interleukin (IL)-6 levels (P < 0.05), increased serum glucagon-like peptide 1, and leptin levels (P < 0.05), downregulated the mRNA expressions of fatty acid synthase, peroxisome proliferator-activated receptor, and lipoprotein lipase (P < 0.05), and upregulated the mRNA expressions of fasting-induced adipose factor, nuclear respiratory factor 1, mitochondrial transcription factor A, tumor necrosis factor receptor superfamily member 9, cytochrome-C oxidase IV and free fatty acid receptor 2 (P < 0.05). Sodium propionate also reduced serum IL-1β level (P < 0.05), increased serum peptide YY level (P < 0.05), downregulated the mRNA expressions of acetyl-coenzyme A carboxylase and sterol regulatory element-binding protein 1c (P < 0.05), and upregulated the mRNA expression of transmembrane protein 26 (P < 0.05). Additionally, sodium butyrate decreased average daily feed intake (P < 0.05) downregulated the mRNA expression of myosin heavy-chain (MyHc) Ⅱb (P < 0.05), and upregulated the mRNA expressions of lipase hormone-sensitive, MyHC Ⅱa and carnitine palmitoyltransferase-1α (P < 0.05). Moreover, the metabolic benefits of SCFAs were partly attributed to the reduction of feed intake. Taken together, SCFAs could reduce appetite and fat accumulation via modulating relevant genes and hormones, which might further illustrate the potential mechanisms that underlay the effects of SCFAs on lipid homeostasis and control of body weight. [Display omitted]

Physical inactivity as well as breakfast skipping is known as risk factor for various metabolic diseases, such as obesity and type 2 diabetes. We have previously reported that a breakfast skipping model, in which the timing of feeding is delayed, induces abnormal lipid metabolism by altering the circadian rhythm of lipid metabolism-related genes in rats. The purpose of this study was to elucidate the synergistic effect of physical inactivity and breakfast skipping on lipid metabolism. We adopted sciatic neurectomized rats as physically inactive models, because we confirmed that the rats mildly decreased their spontaneous locomotor activity compared to sham-operated rats. And then the physically inactive model rats were fed a mild high-fat diet during zeitgeber time (ZT) 12–0 in the control group and ZT16–0 in the breakfast skipping group for 11 days. Body weight gain and total food intake were similar in both groups. Breakfast skipping induced a significant visceral fat accumulation, which was not observed in our previous breakfast skipping or physically inactive studies. The mRNA levels of clock and lipogenesis-related genes were altered by breakfast skipping in the liver and epididymal adipose tissue, and serum insulin level was altered by breakfast skipping. These results suggest that physical inactivity and breakfast skipping synergistically induces drastic visceral fat accumulation due to the alteration of circadian clock and lipid metabolism in the liver and adipose tissue. Therefore, regular feeding timing plays an important role in the health of a sedentary modern society.

Background Excessive fat accumulation of pigs is undesirable, as it severely affects economic returns in the modern pig industry. Studies in humans and mice have examined the role of the gut microbiome in host energy metabolism. Commercial Duroc pigs are often fed formula diets with high energy and protein contents. Whether and how the gut microbiome under this type of diet regulates swine fat accumulation is largely unknown. Results In the present study, we systematically investigated the correlation of gut microbiome with pig lean meat percentage (LMP) in 698 commercial Duroc pigs and found that Prevotella copri was significantly associated with fat accumulation of pigs. Fat pigs had significantly higher abundance of P. copri in the gut. High abundance of P. copri was correlated with increased concentrations of serum metabolites associated with obesity, e.g., lipopolysaccharides, branched chain amino acids, aromatic amino acids, and the metabolites of arachidonic acid. Host intestinal barrier permeability and chronic inflammation response were increased. A gavage experiment using germ-free mice confirmed that the P. copri isolated from experimental pigs was a causal species increasing host fat accumulation and altering serum metabolites. Colon, adipose tissue, and muscle transcriptomes in P. copri -gavaged mice indicated that P. copri colonization activated host chronic inflammatory responses through the TLR4 and mTOR signaling pathways and significantly upregulated the expression of the genes related to lipogenesis and fat accumulation, but attenuated the genes associated with lipolysis, lipid transport, and muscle growth. Conclusions Taken together, the results proposed that P. copri in the gut microbial communities of pigs fed with commercial formula diets activates host chronic inflammatory responses by the metabolites through the TLR4 and mTOR signaling pathways, and increases host fat deposition significantly. The results provide fundamental knowledge for reducing fat accumulation in pigs through regulating the gut microbial composition. 8i_LmNceHRNfJRY2rW1K4p Video Abstract

Obesity is a condition associated with the accumulation of excess fat in the body, energy imbalance, lipogenesis, etc., which increases adipose tissue mass through adipogenesis and poses a health risk. Its prevalence has become an economic burden to the health care system and the world at large. One of the alternatives to tackling obesity involves the use of bioactive compounds. We critically examined the effects of Hibiscus sabdariffa extract (HSE) on various parameters associated with the development of obesity such as; the effect of HSE on body weight, the effect of HSE on lipid accumulation, cholesterol metabolism and plasma parameters, the inhibitory effect of HSE on pancreatic lipase, and the effect of HSE on adipocyte differentiation/adipogenesis. This review has gathered reports on the various anti-obesity effects of H. sabdariffa bioactive compounds in cell and animal models, as well as in humans. Available toxicology information on the consumption of H. sabdariffa revealed that its toxicity is dose-dependent and may cause an adverse effect when administered over a long period of time. Reports have shown that H. sabdariffa derived bioactive compounds are potent in the treatment of obesity with an evident reduction in body weight, inhibition of lipid accumulation and suppression of adipogenesis through the PPARγ pathway and other transcriptional factors.

Recent reports suggest that obesity is caused by dysbiosis of gut microbiota and that it could be prevented or treated through improvement in the composition and diversity of gut microbiota. In this study, high-fat diet (HFD)-induced obese mice were orally administered with Lactobacillus plantarum K50 (K50) isolated from kimchi and Lactobacillus rhamnosus GG (LGG) as a positive control for 12 weeks. Body weight and weights of epididymal, mesenteric, and subcutaneous adipose tissues and the liver were significantly reduced in K50-treated HFD-fed mice compared with HFD-fed mice. The serum triglyceride level was decreased and high-density lipoprotein cholesterol level was increased in K50-treated HFD-fed mice. The gut microbiota analysis showed that the L. plantarum K50 treatment reduced the Firmicutes/Bacteroidetes ratio and improved the gut microbiota composition. In addition, the level of total short-chain fatty acids (SCFAs) in K50-treated HFD-fed mice was higher than that in HFD-fed mice. A remarkable reduction in the fat content of adipose tissue and liver was also observed in K50-treated HFD-fed mice, accompanied by improvements in gene expression related to lipid metabolism, adipogenesis, and SCFA receptors. K50-treated mice had downregulated expression levels of genes and proteins such as TNFα and IL-1β. Our findings confirm that L. plantarum K50 could be a good candidate for ameliorating fat accumulation and low-grade inflammation in metabolic tissues through gut microbiota improvement.

Massive rotator cuff tears (MRCTs) of the shoulder cause disability and pain among the adult population. In chronic injuries, the tendon retraction and subsequently the loss of mechanical load lead to muscle atrophy, fat accumulation, and fibrosis formation over time. The intrinsic repair mechanism of muscle and the successful repair of the torn tendon cannot reverse the muscle degeneration following MRCTs. To address these limitations, we developed an electroconductive matrix by incorporating graphene nanoplatelets (GnPs) into aligned poly(l-lactic acid) (PLLA) nanofibers. This study aimed to understand 1) the effects of GnP matrices on muscle regeneration and inhibition of fat formation in vitro and 2) the ability of GnP matrices to reverse muscle degenerative changes in vivo following an MRCT. The GnP matrix significantly increased myotube formation, which can be attributed to enhanced intracellular calcium ions in myoblasts. Moreover, the GnP matrix suppressed adipogenesis in adipose-derived stem cells. These results supported the clinical effects of the GnP matrix on reducing fat accumulation and muscle atrophy. The histological evaluation showed the potential of the GnP matrix to reverse muscle atrophy, fat accumulation, and fibrosis in both supraspinatus and infraspinatus muscles at 24 and 32 wk after the chronic MRCTs of the rat shoulder. The pathological evaluation of internal organs confirmed the long-term biocompatibility of the GnP matrix. We found that reversing muscle degenerative changes improved the morphology and tensile properties of the tendon compared with current surgical techniques. The long-term biocompatibility and the ability of the GnP matrix to treat muscle degeneration are promising for the realization of MRCT healing and regeneration.

The potential role of the gut microbiota in various human diseases has attracted considerable attention worldwide. Here, we discuss the vital role of the intestinal microbiota in the development of obesity. First, we describe how the gut microbiota promotes fat accumulation. Additionally, a high-fat diet leads to structural instability among in the gut microbiota, further leading to an increase in endotoxins, which aggravates obesity. We then discuss how gut microbiota metabolites, including short-chain fatty acids and lipopolysaccharides, affect the host. Finally, we review several strategies for regulating the intestinal flora.

BackgroundBlack soldier fly (BSF, Hermetia illucens L.) can efficiently degrade organic wastes and transform into a high fat containing insect biomass that could be used as feedstock for biodiesel production. Meanwhile, the molecular regulatory basis of fat accumulation by BSF is still unclear; it is necessary to identify vital genes and regulators that are involved in fat accumulation.ResultsThis study analyzed the dynamic state of fat content and fatty-acid composition of BSF larvae in eight different stages. The late prepupa stage exhibited the highest crude fat, with lauric acid being the main component. Therefore, to provide insight into this unexplained phenomenon, the molecular regulation of rapid fat accumulation by BSF larvae was investigated. The twelve developmental stages of BSF were selected for transcriptome analysis, including the eight stages used for investigation of fat content and fatty-acid composition. By Illumina sequencing, 218,295,450,000 nt were generated. Through assembly by Trinity, 70,475 unigenes were obtained with an average length of 1064 nt and an N50 of 1749 nt. The differentially expressed unigenes were identified by DESeq, with 9159 of them being up-regulated and 10,101 of them were down-regulated. The several putative genes that are involved in the formation of pyruvate, acetyl-CoA biosynthesis, acetyl-CoA transcription, fatty-acid biosynthesis, and triacylglycerol biosynthesis were identified. The four vital metabolic genes that are associated with fat accumulation were validated by quantitative real-time PCR (qRT-PCR). The molecular mechanism of fat accumulation in BSF was clarified in this investigation through the construction of a detailed fat accumulation model from our results.ConclusionThe study provides an unprecedented level of insight from transcriptome sequencing to reveal the crude fat accumulation mechanism in developing BSF. The finding holds considerable promise for insectival biodiesel production, and the fat content and fatty-acid composition can be altered by genetic engineering approaches in the future for the insect production industry.

HFD (high-fat diet) induces obesity and metabolic disorders, which is associated with the alteration in gut microbiota profiles. However, the underlying molecular mechanisms of the processes are poorly understood. In this study, we used the simple model organism honey bee to explore how different amounts and types of dietary fats affect the host metabolism and the gut microbiota. Excess dietary fat, especially palm oil, elicited higher weight gain, lower survival rates, hyperglycemic, and fat accumulation in honey bees. However, microbiota-free honey bees reared on high-fat diets did not significantly change their phenotypes. Different fatty acid compositions in palm and soybean oil altered the lipid profiles of the honey bee body. Remarkably, dietary fats regulated lipid metabolism and immune-related gene expression at the transcriptional level. Gene set enrichment analysis showed that biological processes, including transcription factors, insulin secretion, and Toll and Imd signaling pathways, were significantly different in the gut of bees on different dietary fats. Moreover, a high-fat diet increased the relative abundance of Gilliamella, while the level of Bartonella was significantly decreased in palm oil groups. This study establishes a novel honey bee model of studying the crosstalk between dietary fat, gut microbiota, and host metabolism.