egg-white and Insulin-Resistance

Excessive formation of tumor necrosis factor-α (TNF-α), a pro-inflammatory cytokine, has been implicated in the development of insulin resistance in obesity and type-2 diabetes. In skeletal muscle, chronic exposure to TNF-α impairs insulin-stimulated glucose uptake and insulin signaling. The aim of this study is to investigate the effects of enzymatic egg white hydrolysate (EWH) and its responsible peptide, IRW, on TNF-α-induced insulin resistance and the underlying molecular mechanisms using rat skeletal muscle cells (L6 cells).. Insulin resistance was induced by treating L6 cells with 5 ng/ml TNF-α for 24 h. Effects of EWH and IRW on glucose uptake were detected by glucose uptake assay, glucose transporter 4 (GLUT4) translocation by immunofluorescence, and western blot, while insulin-signaling pathway and mitogen-activated protein kinase (MAPK) pathway were investigated using western blot.. Adding both EWH and IRW significantly improved glucose uptake in TNF-α-treated cells, increased activation of insulin receptor substrate (IRS-1) tyrosine residue and protein kinase B (Akt), whereas decreased activation of IRS-1 serine residue. In addition, TNF-α-induced activation of p38-mitogen-activated protein kinase (p38) and c-Jun N-terminal kinases (JNK) 1/2 were decreased by either EWH or IRW treatment.. EWH and IRW improve impaired insulin sensitivity by down-regulating the activation of p38 and JNK1/2 in TNF-α-treated skeletal muscle cells.

Topics: Animals; Biological Transport; Cells, Cultured; Egg White; Insulin Resistance; Mitogen-Activated Protein Kinases; Muscle Fibers, Skeletal; Peptides; Rats; Tumor Necrosis Factor-alpha

Agents that block the renin-angiotensin system (RAS) improve glucoregulation in the metabolic syndrome disorder. We evaluated the effects of egg white hydrolysate (EWH), previously shown to modulate the protein abundance of RAS component in vivo, on glucose homeostasis in diet-induced insulin-resistant rats. Sprague-Dawley rats were fed a high-fat diet (HFD) for 6 weeks to induce insulin resistance. They were then randomly divided into four groups receiving HFD or HFD supplemented with different concentrations of EWH (1, 2 and 4 %) for another 6 weeks in the first trial. In the second trial, insulin-resistant rats were divided into two groups receiving only HFD or HFD+4 % EWH for 6 weeks. Glucose homeostasis was assessed by oral glucose tolerance and insulin tolerance tests. Insulin signalling and protein abundance of RAS components, gluconeogenesis enzymes and PPARγ were evaluated in muscle, fat and liver. Adipocyte morphology and inflammatory markers were evaluated. In vivo administration of EWH increased insulin sensitivity, improved oral glucose tolerance (P < 0·0001) and reduced systemic inflammation (P < 0·05). EWH potentiated insulin-induced Akt phosphorylation in muscle (P = 0·0341) and adipose tissue (P = 0·0276), but minimal differences in the protein abundance of tissue RAS components between the EWH and control groups were observed. EWH treatment also reduced adipocyte size (P = 0·0383) and increased PPARγ2 protein abundance (P = 0·0237). EWH treatment yielded positive effects on the inflammatory profile, glucose tolerance, insulin sensitivity and adipocyte differentiation in HFD-induced insulin resistance rats. The involvement of local RAS activity requires further investigation.

Topics: Adipocytes; Adipose Tissue; Animal Feed; Animals; Biomarkers; Blood Glucose; Diet, High-Fat; Egg White; Gluconeogenesis; Glucose; Glucose Tolerance Test; Homeostasis; Inflammation; Insulin Resistance; Male; Rats; Rats, Sprague-Dawley; Renin-Angiotensin System

The purpose of this study was to evaluate the effect of the administration of two egg white hydrolysates on glucose metabolism complications related to Metabolic Syndrome (MS) in Zucker fatty rats (ZFR). ZFR were given 750 mg/kg/day of egg white hydrolyzed with pepsin (HEW1) or with aminopeptidase (HEW2) for 12 weeks in their drinking water or just water. Zucker lean rats (ZLR), which received water, were used as a control. The presence of tactile allodynia, which is a sign of peripheral neuropathy, was assessed. Blood samples and pancreas were collected to determine the effect of the hydrolysates on glucose metabolism. The intake of HEW1 significantly lowered plasma insulin levels and improved the quantitative indexes of insulin resistance, insulin sensitivity, and pancreatic β-cell functionality (HOMA-IR, HOMA-β, and QUICKI, respectively), but non-significant changes were observed in group treated with HEW2. Compared to ZLR, ZFR showed tactile allodynia, but the consumption of both hydrolysates significantly increased mechanical sensitivity in ZFR. In conclusion, HEW1 pepsin could improve the glucose metabolism abnormalities associated with MS in obese Zucker rats.

Topics: Animals; Blood Glucose; Egg White; Hyperalgesia; Insulin; Insulin Resistance; Insulin-Secreting Cells; Male; Metabolic Syndrome; Ovalbumin; Pepsin A; Peripheral Nervous System Diseases; Protein Hydrolysates; Rats, Zucker

We have previously reported that chicken egg white (EW) and low-allergenic EW hydrolysate (EWH) suppressed ectopic fat accumulation and improved serum glucose and insulin levels. In this study, the dietary effects of EW and EWH on glucose tolerance were investigated in different ways to clarify the effect of EW and EWH on intestinal glucose absorption. Type 2 diabetic Nagoya-Shibata-Yasuda mice were divided into four groups: a low-fat and low-sucrose casein-based diet group (NL); high-fat and high-sucrose (HFS) casein-based diet group (NH); HFS EW-based diet group (NE); and HFS EWH-based diet group (NEH). Mice were fed their respective diets for 8 wk. At the end of the 6th and 7th week, an oral glucose tolerance test (OGTT) and insulin tolerance test (ITT) were respectively conducted in experiment A. At the end of the 7th week, an intraperitoneal glucose tolerance test (ipGTT) was conducted in experiment B. In experiment A, the plasma glucose level was suppressed in the NE group during both OGTT and ITT, and suppressed in the NEH group during OGTT, but not during ITT. In experiment B, the plasma glucose level was similarly suppressed in the NEH group during ipGTT, but the suppressive effect was weakened compared to OGTT. Plasma insulin level was lower in the NE and NEH groups in both experiments. Fecal triacylglycerol excretion was increased in the NE and NEH groups in experiment A and liver triacylglycerol content was suppressed in the NE group in experiment B. These findings suggested that in addition to improving fat metabolism, EWH improves glucose tolerance via mechanisms related and unrelated to small intestinal function.

Topics: Animals; Blood Glucose; Caseins; Diabetes Mellitus, Type 2; Dietary Fats; Dietary Sucrose; Egg White; Feces; Glucose; Glucose Tolerance Test; Insulin Resistance; Intestinal Absorption; Liver; Male; Mice; Mice, Inbred ICR; Protein Hydrolysates; Triglycerides

We investigated the fat metabolic characteristics in non-obese and diabetic Goto-Kakizaki (GK) rat and the effects of dietary egg white hydrolysate (EWH) on glucose and fat metabolism. Wistar (W) and GK (G) rats were placed into dietary casein (WC and GC) or EWH (WE and GE) group, and fed their respective diet for six weeks. Triglyceride (TG) content and stearoyl-CoA desaturase (SCD) indices in the soleus muscle were higher in the GC group than WC group in parallel with worsening serum glucose metabolic parameters. The glucose metabolic parameters were significantly improved in the GE group. The TG accumulation and SCD indices in the soleus muscle were also significantly lower in the GE group than in the GC group. In conclusion, dietary EWH not only improved glucose metabolism but also reduced both TG accumulation and SCD indices in the soleus muscle of GK rat.

Topics: Animals; Blood Glucose; Diabetes Mellitus, Type 2; Down-Regulation; Egg Proteins, Dietary; Egg White; Hyperglycemia; Hypertriglyceridemia; Hypoglycemic Agents; Hypolipidemic Agents; Insulin Resistance; Male; Muscle, Skeletal; Protein Hydrolysates; Rats, Inbred Strains; Rats, Wistar; Stearoyl-CoA Desaturase; Triglycerides