Lycium barbarum polysaccharide ameliorates the accumulation of lipid droplets in adipose tissue via an ATF6/SIRT1-dependent mechanism.

Lipid droplets (LDs) are dynamic organelles that store neutral lipids and are closely linked to obesity. Previous studies have suggested that Lycium barbarum polysaccharide (LBP) supplements can ameliorate obesity, but the underlying mechanisms remain unclear. In this study, we hypothesize that LBP alleviates LD accumulation in adipose tissue (AT) by inhibiting fat-specific protein 27 (Fsp27) through an activating transcription factor-6 (ATF6)/small-molecule sirtuin 1 (SIRT1)-dependent mechanism. LD accumulation in AT is induced in high-fat diet (HFD)-fed mice, and differentiation of 3T3-L1 preadipocytes (PAs) is induced. The ability of LBP to alleviate LD accumulation and the possible underlying mechanism are then investigated both in vivo and in vitro. The influences of LBP on the expressions of LD-associated genes ( ATF6 and Fsp27) are also detected. The results show that HFD and PA differentiation markedly increase LD accumulation in ATs and adipocytes, respectively, and these effects are markedly suppressed by LBP supplementation. Furthermore, LBP significantly activates SIRT1 and decreases ATF6 and Fsp27 expressions. Interestingly, the inhibitory effects of LBP are either abolished or exacerbated when ATF6 is overexpressed or silenced, respectively. Furthermore, SIRT1 level is transcriptionally regulated by LBP through opposite actions mediated by ATF6. Collectively, our findings suggest that LBP supplementation alleviates obesity by ameliorating LD accumulation, which might be partially mediated by an ATF6/SIRT1-dependent mechanism.

Causal relationship between insulin resistance and sarcopenia.

Sarcopenia is a multifactorial disease characterized by reduced muscle mass and function, leading to disability, death, and other diseases. Recently, the prevalence of sarcopenia increased considerably, posing a serious threat to health worldwide. However, no clear international consensus has been reached regarding the etiology of sarcopenia. Several studies have shown that insulin resistance may be an important mechanism in the pathogenesis of induced muscle attenuation and that, conversely, sarcopenia can lead to insulin resistance. However, the causal relationship between the two is not clear. In this paper, the pathogenesis of sarcopenia is analyzed, the possible intrinsic causal relationship between sarcopenia and insulin resistance examined, and research progress expounded to provide a basis for the clinical diagnosis, treatment, and study of the mechanism of sarcopenia.

Microecological preparation combined with an modified low-carbon diet improves glucolipid metabolism and cardiovascular complication in obese patients.

OBJECTIVE: To investigate the impact of microecological preparation combined with modified low-carbon diet on the glucolipid metabolism and cardiovascular complication in obese patients. METHODS: From August 2017 to July 2020, 66 obese patients were recruited, and administrated with an modified low-carbon diet with (group A) or without (Group B) microecology preparation and a balanced diet in control group (group C) for 6 months. Meanwhile, 20 volunteers administrated with a balanced diet were recruited as the healthy control group (group D). RESULTS: After 6-month intervention, obese subjects in group A and B showed significant improvement of body and liver fat mass, reduction of serum lipid levels, intestinal barrier function markers, insulin resistance index (IRI), high blood pressure (HBP) and carotid intima thickness, as compared with subjects in group C. More importantly, subjects in group A had better improvement of vascular endothelial elasticity and intimal thickness than subjects in group B. However, these intervention had no effect on carotid atherosclerotic plaque. CONCLUSION: Administration of microecological preparation combined with modified low-carbon diet had better improvement of intestinal barrier function, glucose and lipid metabolism, and cardiovascular complications than low-carbon diet in obese patients, but the effect of a simple low-carb diet on carotid atherosclerotic plaque need to be further addressed.

Effects of marine collagen peptides on glucose metabolism and insulin resistance in type 2 diabetic rats.

The present study was conducted to investigate the effects of marine collagen peptides (MCPs) on glucose metabolism and insulin resistance using a rat model of type 2 diabetes mellitus (T2DM). Forty T2DM obese Wistar rats were randomly assigned to receive varying doses of MCPs or a vehicle control for 4 weeks. Blood glucose and insulin levels, as well as oxidative stress and inflammation were measured. The expression of glucose transporter type 4 (GLUT4) in skeletal muscles and peroxisome proliferator-activated receptor-α (PPAR-α) in livers of T2DM rats was also measured. It was found that in the group of 9.0 g/kg/day MCPs significantly improved glucose, insulin, and homeostatic model assessment-insulin resistance, and increased the insulin sensitivity index (ISI). In addition, the groups of 4.5 and 2.25 g/kg/day MCPs significantly improved liver steatosis. It was also found that MCPs decreased expression of oxidative stress biomarkers and inflammatory cytokines and adipocytokines in T2DM rats. In conclusion, medium and high doses of MCPs (≥4.5 g/kg/day) improved glucose metabolism and insulin sensitivity in T2DM rats. These beneficial effects of MCPs may be mediated by decreasing oxidative stress and inflammation and by up-regulating GLUT4, and PPAR-α activity.

Marine collagen peptides reduce endothelial cell injury in diabetic rats by inhibiting apoptosis and the expression of coupling factor 6 and microparticles.

The present study aimed to elucidate the role of marine collagen peptides (MCPs) in protection of carotid artery vascular endothelial cells (CAVECs) in type 2 diabetes mellitus (T2DM), and the mechanism underlying this process. In an in vivo experiment, diabetic Wistar rats were divided randomly into four groups (n=10/group): Diabetes control, and three diabetes groups administered low, medium and high doses of MCPs (2.25, 4.5 and 9.0 g/kg body weight/day, respectively). Another 10 healthy rats served as the control. In an in vitro experiment, human umbilical­vein endothelial cells (HUVECs) were incubated in normal and high concentrations of glucose with or without MCPs (3.0, 15.0 and 30.0 mg/ml, respectively) for 24, 48 or 72 h. Blood vessel/endothelial construction, inflammatory exudation and associated molecular biomarkers in CAVECs were detected and analyzed. The results of the present study demonstrated that in rats, MCP treatment for 4 weeks significantly lowered blood glucose and attenuated endothelial thinning and inflammatory exudation in carotid­artery vascular endothelial cells. In vitro, the high­glucose intervention significantly increased cell apoptosis in HUVECs, and medium and high doses of MCPs (4.5 and 9.0 g/kg body weight/day, respectively) partially ameliorated this high glucose­mediated apoptosis and decreased levels of apoptosis biomarkers. In conclusion, a moderate oral MCP dose (≥4.5 g/kg body weight/day) may be a novel therapeutic tool to protect against early cardiovascular complications associated with T2DM by inhibiting apoptosis and reducing the expression of coupling factor 6 and microparticles.

Treatment with marine collagen peptides modulates glucose and lipid metabolism in Chinese patients with type 2 diabetes mellitus.

This study was aimed at examining the therapeutic effects of marine collagen peptides (MCPs) from fish hydrolysate in Chinese patients with type 2 diabetes mellitus (T2DM). A total of 100 diabetic patients and 50 healthy controls were recruited. Diabetic patients were randomized into treatment and control groups. The patients in the treatment group received an additional 13 g of MCPs daily for 3 months. Their blood samples were collected before, and 1.5 and 3 months after, treatment to evaluate glucose and lipid metabolism. The levels of serum high-sensitivity C-reactive protein (hs-CRP), nitric oxide (NO), bradykinin, prostacyclin (PGI2), and adipokines were determined. Significantly reduced levels of fasting blood glucose, human glycated hemoglobin A1c (GHbA1c), fasting blood insulin, total triglycerides, total cholesterol, low-density lipoprotein, and free-fatty acids, but increased levels of insulin sensitivity index and HDL were observed in T2DM patients following treatment with MCPs for 1.5 and 3 months. The values of these measures were significantly lower or higher than those of patient controls (p < 0.01), respectively. Interestingly, significantly decreased levels of hs-CRP and NO, but increased levels of bradykinin, PGI2, and adiponectin were detected in MCP-treated T2DM patients (p < 0.01), as compared with their basal values or the levels in patient controls. MCP treatment improved glucose and lipid metabolism in diabetic patients.

Therapeutic effects of marine collagen peptides on Chinese patients with type 2 diabetes mellitus and primary hypertension.

INTRODUCTION: Marine collagen peptides (MCPs) from deep sea fish are shown to ameliorate hyperlipidemia in animal models. The study aimed at examining the effects of MCPs on glucose and lipid metabolism in Chinese patients with type 2 diabetes mellitus (T2DM) and primary hypertension. METHODS: One hundred patients with T2DM and primary hypertension and 50 healthy subjects (normal controls) were recruited for a randomized double blind study. The patients were randomized into MCPs treatment or patient control groups (n = 50 per group). Both patient controls and normal controls were given carboxymethylcellulose twice daily whereas the MCPs treatment group was given MCPs twice daily for 3 months. Blood pressure, glucose and lipid metabolism, serum high-sensitivity C-reactive protein, cytochrome P450, nitric oxide, bradykinin, prostacyclin, creatinine, uric acid and adipokines were measured at baseline, 1.5 and 3 months after treatment. All patients received regular medicines for control of hyperglycemia and hypertension. RESULTS: Compared with patient controls, significantly reduced levels of fasting blood glucose, HbA1c, diastolic blood pressure, mean arterial pressure and creatinine but increased levels of Insulin Sensitivity Index and Insulin Secretion Index were observed in patients receiving MCPs treatment. Furthermore, significantly reduced levels of serum triglycerides, total cholesterol, low-density lipoprotein, free fatty acids, cytochrome P450, nitric oxide and prostacyclin but increased levels of high-density lipoprotein, bradykinin and adiponectin were detected in patients taking MCPs. CONCLUSIONS: MCPs supplement may benefit glucose and lipid metabolism, insulin sensitivity, renal function and hypertension management in Chinese patients with T2DM and hypertension.

Effect of marine collagen peptides on markers of metabolic nuclear receptors in type 2 diabetic patients with/without hypertension.

OBJECTIVE: To explore Effects of marine collagen peptides (MCPs) on markers of metablic nuclear receptors, i.e peroxisome proliferator-activated receptor (PPARs), liver X receptor (LXRs) and farnesoid X receptor (FXRs) in type 2 diabetic patients with/without hypertension. METHOD Study population consisted of 200 type 2 diabetic patients with/without hypertension and 50 healthy subjects, all of whom were randomly assigned to MCPs-treated diabetics (n = 50), placebo-treated diabetics (n = 50), MCPs-treated diabetics with hypertension (n=50), placebo-treated diabetics with hypertension (n = 50), and healthy controls (n = 50). MCPs or placebo (water-soluble starch) were given daily before breakfast and bedtime over three months. Levels of free fatty acid, cytochrome P450, leptin, resistin, adiponectin, bradykinin, NO, and Prostacyclin were determined before intervention, and 1.5 months, and 3 months after intervention. Hypoglycemia and the endpoint events during the study were recorded and compared among the study groups. RESULT: At the end of the study period, MCPs-treated patients showed marked improvement compared with patients receiving placebo. The protection exerted by MCPs seemed more profound in diabetics than in diabetics with hypertension. In particular, after MCPs intervention, levels of free fatty acid, hs-CRP, resistin, Prostacyclin decreased significantly in diabetics and tended to decrease in diabetic and hypertensive patients whereas levels of cytochrome P450, leptin, NO tended to decrease in diabetics with/without hypertension. Meanwhile, levels of adiponectin and bradykinin rose markedly in diabetics following MCPs administration. CONCLUSION: MCPs could offer protection against diabetes and hypertension by affecting levels of molecules involved in diabetic and hypertensive pathogenesis. Regulation on metabolic nuclear receptors by MCPs may be the possible underlying mechanism for its observed effects in the study. Further study into its action may shed light on development of new drugs based on bioactive peptides from marine sources.

Beneficial effects of oligopeptides from marine salmon skin in a rat model of type 2 diabetes.

OBJECTIVE: This study aimed at investigating whether treatment with oligopeptides from marine salmon skin (OMSS) could modulate type 2 diabetes mellitus (T2DM)-related hyperglycemia and ß-cell apoptosis in rats induced by high fat diet and low doses of streptozotocin and its therapeutic mechanisms. METHODS: Groups of T2DM rats were treated with OMSS or bovine serum albumin (3.0 g/kg/d) for 4 wk and their blood samples, together with those of normal control rats, were collected before and 4 wk after treatment. The levels of fasting blood glucose (FBG) and insulin, serum superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione (GSH), tumor necrosis factor-alpha (TNFα), and interferon-gamma (IFNγ) in rats were determined. The islet cell apoptosis and Fas/FasL expression were detected by TUNEL and immunohistochemistry. RESULTS: In comparison with control rats, higher levels of FBG and frequency of apoptotic islet cells were detected in the bovine serum albumin group of diabetic rats, accompanied by higher levels of Fas expression in the pancreatic islets, serum TNFα, IFNγ, and MDA, but lower levels of SOD and GSH. However, the levels of FBG and frequency of apoptotic islet cells were significantly reduced in OMSS-treated rats. Lower levels of Fas expression were observed in the pancreatic islets of OMSS-treated rats. Significantly reduced levels of serum TNFα, IFNγ, and MDA, but increased levels of SOD and GSH, were detected in OMSS-treated rats. CONCLUSIONS: Treatment with OMSS significantly reduced FBG in diabetic rats. This antidiabetic activity may be mediated by down-regulating T2DM-related oxidative stress and inflammation, protecting the pancreatic ß-cells from apoptosis.