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Curcumin is an active component derived from Curcuma longa L. which is a traditional Chinese medicine that is widely used for treating metabolic diseases through regulating different molecular pathways. Here, in this study, we aimed to comprehensively investigate the effects of curcumin on glycolipid metabolism in vivo and in vitro and then determine the underlying mechanism. Male C57BL/6 J obese mice and 3T3-L1 adipocytes were used for in vivo and in vitro study, respectively. Our results demonstrated that treatment with curcumin for eight weeks decreased body weight, fat mass and serum lipid profiles. Meanwhile, it lowered fasting blood glucose and increased the insulin sensitivity in high-fat diet-induced obese mice. In addition, curcumin stimulated lipolysis and improved glycolipid metabolism through upregulating the expressions of adipose triglyceride lipase and hormone-sensitive lipase, peroxisome proliferator activated receptor γ/α (PPARγ/α) and CCAAT/enhancer binding proteinα (C/EBPα) in adipose tissue of the mice. In differentiated 3T3-L1 cells, curcumin reduced glycerol release and increased glucose uptake via upregulating PPARγ and C/EBPα. We concluded that curcumin has the potential to improve glycolipid metabolism disorders caused by obesity through regulating PPARγ signalling pathway., Competing Interests: We declare we have no competing interests.

We deduced that leukocyte-derived H 2 S would also play a pivotal role regarding nutrition homeostasis in hypertensive subjects. Plasma was obtained from patients with hypertension (n  =  151) as well as control (n  =  41). Leukocyte-derived H 2 S speed was determined, and biochemical indices of glucose and lipid metabolism were measured. Western blot analyses of CSE were also performed. Inflammation factors were measured. Leukocyte-derived H 2 S is produced at a significantly lower rate in overweight or obese patients (p < 0.05). There is a significant negative correlation between H 2 S and the levels of HOMA-RI and insulin in overweight patients and has a positive relationship with HDL-C only in overweight hypertensive patients (p < 0.05). Patients with high insulin levels showed down-regulation of CSE (p < 0.05). The levels of IL-10 decreased in both the obese and the overweight which showed significant relationship with all metabolism parameters such as HDL-C(r = 0.176, p = 0.031), insulin (r = -0.181, p = 0.027), HOMA-IR (r = -0.166, p = 0.045), and H 2 S speed (r = 0.995, p = 0.001). Linear regression analysis showed that insulin levels will increase (β = -1.685, p = 0.041) with the slower speed of H 2 S. Leukocyte-derived H 2 S production varied according to the nutritional status of hypertensive subjects, and the H 2 S/IL-10 signaling pathway may be the junction point among hypertension, disturbance of nutritional status, and inflammation.

This study aimed to evaluate the effects of Zanthoxylum alkylamides on the glycolipid metabolism of rats with streptozotocin (STZ)-induced diabetes. Diabetic rats were given daily oral treatments of 2, 4, or 8 mg/kg bw alkylamides for 28 days. Alkylamides significantly decreased fasting blood glucose and fructosamine content, as well as relieved organ enlargement caused by diabetes. The serum and liver triglyceride, malondialdehyde, and free fatty-acid contents of rats with STZ-induced diabetes were significantly reduced. Total cholesterol in the liver also significantly decreased. Quantitative polymerase chain reaction (Q-PCR) and Western blot detected insignificantly increased (P > 0.05) mRNA expression levels of adenosine monophosphate-activated protein kinase (AMPK) in the skeletal muscle of diabetic rats. However, AMPK and p-AMPK (Thr172) protein expression levels significantly increased. The mRNA and protein expression levels of silencing information regulator 1 significantly increased. The mRNA expression levels of acetyl-CoA-carboxylase (ACC) and protein p-ACC (Ser79) also increased. The mRNA and protein expression levels of glucose transporter type 4 (GLUT4) were significantly upregulated in the skeletal muscle cell membranes of diabetic rats. Results indicated that alkylamides activated the AMPK-signaling pathway. Thus, inhibiting ACC activity reduced fatty-acid synthesis. The rapid translocation of GLUT4 mediated increased glucose transport rate and reduced blood glucose. Therefore, alkylamides can ameliorate glucose and lipid metabolism disorders in diabetic rats by activating the AMPK pathway.

To explore the effects of hesperidin on glycolipid metabolic disorders and its mechanism in mice induced by high-fat diet, 40 male C57 mice were randomly divided into control group, OB group, low dose group (OB+ hes-low) and high dose group (OB+ hes-high) according to the diet. After 16 weeks, the body weight, liver index and visceral fat index in all mice were detected. The glucose metabolism indications (blood glucose, insulin levels and HOMA-IR) and serum lipid levels were evaluated. The mRNA expression of insulin signaling pathway genes(IR, IRS1, Glut2, Glut4), lipid metabolism pathway genes(SREBP-1c, FAS, ACC, PPARα) and AMPK were analyzed by Real-time PCR. After 16-week feeding, the indicators in OB group were higher than those in control group, including body weight, body fat deposition, serum glucose, serum lipid, serum insulin and HOMA-IR index (P<0.05). And impaired glucose tolerance occurred in the OB group (P<0.05). Treating with hesperidin, whether in low or high dose, attenuated these changes (P<0.05), especially in high dose group(P<0.05). Hesperidin, especially in high dose, upregulated the mRNA expressions of AMPK (P<0.05), which had impact on the gene expressions of insulin signaling pathway (IR, IRS-1, Glut2/4) (P<0.05) and lipid metabolism related genes (SREBP-1c and Fas and ACC) (P<0.05). The activatory effect of hesperidin on the mRNA expressions of PPARα was also observed (P<0.05), especially in high dose group (P<0.05). Hesperidin inhibits obesity, hyperglycemia, hyperlipemia and attenuates insulin resistance. These effects might be closed related to the activation of AMPK, which regulate the insulin signaling pathway and lipid metabolism., Competing Interests: The authors of this article and the planning committee members and staff have no relevant financial relationships with commercial interests to disclose., (Copyright© by the Chinese Pharmaceutical Association.)

Basic data on the resting energy expenditure (REE) of healthy populations are currently rare, especially for developing countries. The aims of the present study were to describe gender- and age-specific REE distributions and to evaluate the relationships among glycolipid metabolism, eating behaviors, and REE in healthy Chinese adults. This cross-sectional survey included 540 subjects (343 women and 197 men, 20-79 years old). REE was measured by indirect calorimetry and expressed as kcal/day/kg total body weight. The data were presented as the means and percentiles for REE and the REE to fat-free mass (FFM) ratio; differences were described by gender and age. Partial correlation analysis was used to analyze the correlations between REE, tertiles of REE/FFM, and glycolipid metabolism and eating behaviors. In this study, we confirmed a decline in REE with age in women (p = 0.000) and men (p = 0.000), and we found that men have a higher REE (p = 0.000) and lower REE/FFM (p = 0.021) than women. Furthermore, we observed no associations among glycolipid metabolism, eating behaviors, and REE in healthy Chinese adults. In conclusion, the results presented here may be useful to clinicians and nutritionists for comparing healthy and ill subjects and identifying changes in REE that are related to aging, malnutrition, and chronic diseases., Competing Interests: The authors declare no conflicts of interest.

Introduction: The aim of the study was to investigate the effects of metformin and sitagliptin on glycolipid metabolism in type 2 diabetes after different diets., Material and Methods: Seventy Male Sprague Dawley rats were fed with a high fat diet followed by streptozotocin treatment to induce type 2 diabetes. Then all rats were randomly divided into a control group, a metformin group (200 mg/kg), and a sitagliptin group (10 mg/kg). Each group was further divided into 4 groups receiving one load of high carbohydrate diet (45% glucose, 4.5 ml/kg), high fat diet (20% lipid emulsion, 4.5 ml/kg), high protein diet (20% whey protein, 10 ml/kg) or mixed meal, respectively. The caloric densities were all 33 kJ/kg. Postprandial blood glucose (P2BG), triglyceride (TG), glucagon-like peptide-1 (GLP-1), glucagon and insulin levels were measured., Results: In the high carbohydrate group, sitagliptin was more efficient in lowering P2BG compared with metformin (p < 0.05). In the high-fat group, metformin was more powerful in lowering TG (p < 0.05) and P2BG (p < 0.05) levels because of its improvement of insulin sensitivity. In the high protein diet group, metformin did not reduce the P2BG level (p > 0.05), although it did reduce the TG level (p < 0.05). In the mixed diet group, metformin was more efficient in lowering P2BG (p < 0.05) but had a similar effect on TG (p > 0.05) compared with sitagliptin., Conclusions: In the type 2 diabetic model, metformin and sitagliptin have different effects on glycolipid metabolism after different diets. If it is proved in type 2 diabetic patients, then different medicines may be recommended according to different diets in order to improve glycolipid metabolism.