The insulin sensitivity response is determined by the interaction between the G972R polymorphism of the insulin receptor substrate 1 gene and dietary fat

Scope : Insulin resistance, a condition associated with type 2 diabetes mellitus, results from the interaction of environmental and genetic factors. The aim of this study was to explore the influence of the G972R polymorphism at the insulin receptor substrate 1 gene on insulin sensitivity in a healthy young population. Furthermore, we examined whether the presence of this single nucleotide polymorphism (SNP; GR or GG) interacts with dietary fat to modulate insulin sensitivity. Methods and results : Fifty‐nine healthy volunteers consumed three diets during 4 wk each following a randomized crossover design: a saturated fatty acid diet, a low‐fat and high carbohydrate (CHO) diet or a MUFA diet. For each diet, we investigated peripheral insulin sensitivity with the insulin suppression test. Steady‐state plasma glucose and plasma‐free fatty acids concentrations were significantly lower in GR subjects after the intake of a CHO diet, than did homozygous GG subjects (p<0.05). However, no differences were observed after consuming the two other diets. Conclusions : Insulin sensitivity increased in GR subjects for the G972R polymorphism at the insulin receptor substrate 1 gene locus, after intake of a CHO diet. Increased knowledge of how these and other genes influence insulin sensitivity should increase the understanding of personalized nutrition.     

Improvement of insulin resistance by Hon-Chi in fructose-rich chow-fed rats

In an attempt to develop new substances for handling insulin resistance, the effect Hon-Chi was examined on insulin resistance induced by fructose-rich chow in rats. Mandarin Hon-Chi is red yeast rice fermented with Monascus pilous and Monascus purpureus. Single oral administration of Hon-Chi for 90 min decreased the plasma glucose in a dose-dependent manner in rats, which had received four-week fructose-rich chow. The insulin action on glucose disposal rate using the glucose–insulin index, and the value of the areas under the curve of glucose and insulin during the intraperitoneal glucose tolerance test were measured. Oral administration (three times daily for three-days) of Hon-Chi into rats, which received four-week fructose-rich chow, reversed the elevated value of glucose-insulin index, indicating Hon-Chi has an ability to improve insulin resistance. The time for the loss of plasma glucose lowering response to tolbutamide in fructose-rich chow-fed rats was markedly delayed by the repeated treatment of Hon-Chi, as compared to the vehicle-treated group. This provided the supportive data that oral administration of Hon-Chi could delay the development of insulin resistance in rats. Increase of insulin sensitivity by Hon-Chi was further identified using the plasma glucose lowering action of exogenous insulin in streptozotocin-induced diabetic rats (STZ-diabetic rats). Oral administration of Hon-Chi at 150 mg/kg three times daily into STZ-diabetic rats caused an increase in the responses to exogenous insulin 15-days later. The obtained results suggest that oral administration of Hon-Chi has the ability to improve insulin sensitivity and delay the development of insulin resistance in rats, which may be used as an adjuvant therapy to patients with insulin resistance.     

驴乳抑制胰岛素抵抗形成与氨基酸代谢的相关性

目的探讨驴乳(donkeymilk,DM)抑制高脂饮食诱导的胰岛素抵抗形成与氨基酸代谢的相关性。方法将36只C57BL/6N小鼠随机分为空白对照(Con)组,高脂饮食(high fat diet, HFD)组和HFD+驴乳组。给予空白对照组小鼠普通饲料及生理盐水灌胃, HFD组给予高脂饲料及生理盐水灌胃, HFD+驴乳组给予高脂饲料,并且每天按0.1 mL/10 g驴乳灌胃。饮食和驴乳干预8周后,检测各组小鼠血糖血脂水平和胰岛素敏感性,采用超高效液相色谱-串联质谱测定小鼠血浆靶标氨基酸含量,结合SIMCA-P软件对氨基酸数据进行PLS-DA分析,并分析变化的靶标氨基酸与血糖血脂水平的相关性。结果高脂饮食诱导8周,与Con组小鼠相比,HFD组小鼠体重、随机血糖(glucose, GLU)、总胆固醇(total cholesterol, TC)水平、口服葡萄糖耐量(oral glucose tolerancetest,OGTT)曲线下面积、胰岛素耐量曲线下面积和空腹血清胰岛素水平显著升高(P0.05),胰岛素敏感指数下降(P0.05)。与HFD组相比, HFD+驴乳组体重、GLU、TC和甘油三酯(triglyceride, TG)水平、OGTT曲线下面积显著降低(P0.05)。与空白对照组小鼠比较,HFD组小鼠血清中丙氨酸、半胱氨酸、脯氨酸、甲硫氨酸含量升高,赖氨酸含量降低(P0.05);与HFD组比较,HFD+驴乳组中的半胱氨酸含量显著降低(P0.01)。PLS-DA分析结果显示驴乳给予后小鼠血清氨基酸代谢谱较模型组发生了显著变化。Pearson相关分析显示,脯氨酸、甲硫氨酸和半胱氨酸分别与空腹血糖(fasting blood glucose, FBG)、GLU、TC水平呈显著性正相关(P0.05)。结论驴乳能够延缓高脂饮食诱导小鼠胰岛素抵抗的发生,并且驴乳能够影响胰岛素抵抗小鼠的血清氨基酸代谢谱,被改变的半胱氨酸、脯氨酸、甲硫氨酸的代谢与胰岛素抵抗的发生发展密切相关。     

Semi-modified okara whey diet increased insulin secretion in diabetic rats fed a basal or high fat diet

Food Science and Biotechnology - Lifestyle and diet preferences are primarily responsible for developing type 2 diabetes. In this study, okara was manufactured into okara whey crackers (OWC) to...     

Saffron (Crocus sativus L.) increases glucose uptake and insulin sensitivity in muscle cells via multipathway mechanisms

Saffron (Crocus sativus Linn.) has been an important subject of research in the past two decades because of its various biological properties, including anti-cancer, anti-inflammatory, and anti-atherosclerotic activities. On the other hand, the molecular bases of its actions have been scarcely understood. Here, we elucidated the mechanism of the hypoglycemic actions of saffron through investigating its signaling pathways associated with glucose metabolism in C₂C₁₂ skeletal muscle cells. Saffron strongly enhanced glucose uptake and the phosphorylation of AMPK (AMP-activated protein kinase)/ACC (acetyl-CoA carboxylase) and MAPKs (mitogen-activated protein kinases), but not PI 3-kinase (Phosphatidylinositol 3-kinase)/Akt. Interestingly, the co-treatment of saffron and insulin further improved the insulin sensitivity via both insulin-independent (AMPK/ACC and MAPKs) and insulin-dependent (PI 3-kinase/Akt and mTOR) pathways. It also suggested that there is a crosstalk between the two signaling pathways of glucose metabolism in skeletal muscle cells. These results could be confirmed from the findings of GLUT4 translocation. Taken together, AMPK plays a major role in the effects of saffron on glucose uptake and insulin sensitivity in skeletal muscle cells. Our study provides important insights for the possible mechanism of action of saffron and its potential as a therapeutic agent in diabetic patients.     

Consumption of barley β‐glucan ameliorates fatty liver and insulin resistance in mice fed a high‐fat diet

Consumption of a diet high in barley β‐glucan (BG) has been shown to prevent insulin resistance. To investigate the mechanism for the effects of barley BG, three groups of male 7‐wk‐old C57BL/6J mice were fed high‐fat diets containing 0, 2, or 4% of barley BG for 12 wk. The 2% BG and 4% BG groups had significantly lower body weights compared with the 0% BG group. The 4% BG group demonstrated improved glucose tolerance and lower levels of insulin‐resistance index and glucose‐dependent insulinotropic polypeptide. Consumption of the BG diet decreased hepatic lipid content. Mice on the BG diet also demonstrated decreased fatty acid synthase and increased cholesterol 7α‐hydroxylase gene expression levels. The BG diet promoted hepatic insulin signaling by decreasing serine phosphorylation of insulin receptor substrate 1 and activating Akt, and it decreased mRNA levels of glucose‐6‐phosphatase and phosphoenolpyruvate carboxykinase. In summary, consumption of BG reduced weight gain, decreased hepatic lipid accumulation, and improved insulin sensitivity in mice fed a high‐fat diet. Insulin signaling enhanced due to the expression changes of glucose and lipid metabolism genes by BG consumption. Consumption of barley BG could be an effective strategy for preventing obesity, insulin resistance, and the metabolic syndrome.