Dietary sugars and carbohydrate metabolism in type II diabetes

Diabetes, the most common metabolic disease, is responsible for the deaths of over 300,000 Americans annually. The incidence of the disease increases with age and since the U.S. population is graying, prevalence is also increasing. Obesity and family history are strong predictors of diabetes. The etiology of Type II diabetes is heterogeneous. The hyperglycemia of Type II diabetes can result from a variety of metabolic defects including impaired beta cell secretion, receptor deficiencies, or abnormal hepatic production or uptake of glucose. Other glucoregulatory hormones such as glucagon, growth hormone, cortisol, thyroid hormones, somatostatin, and gastric inhibitory polypeptide may contribute to the aberrations of carbohydrate metabolism. Environmental factors including stress, diet, and exercise may also contribute to the disease. Since most diabetics are obese, weight loss should be the first priority in improving status. A variety of diet and exercise regimens may help achieve this goal or even improve glucose control without weight loss. Due to the heterogeneity of the disease individualized treatment must be used to improve status of patients with the various metabolic defects of Type II diabetes.     

Dietary sugars and carbohydrate metabolism in type II diabetes.

Diabetes, the most common metabolic disease, is responsible for the deaths of over 300,000 Americans annually. The incidence of the disease increases with age and since the U.S. population is graying, prevalence is also increasing. Obesity and family history are strong predictors of diabetes. The etiology of Type II diabetes is heterogeneous. The hyperglycemia of Type II diabetes can result from a variety of metabolic defects including impaired beta cell secretion, receptor deficiencies, or abnormal hepatic production or uptake of glucose. Other glucoregulatory hormones such as glucagon, growth hormone, cortisol, thyroid hormones, somatostatin, and gastric inhibitory polypeptide may contribute to the aberrations of carbohydrate metabolism. Environmental factors including stress, diet, and exercise may also contribute to the disease. Since most diabetics are obese, weight loss should be the first priority in improving status. A variety of diet and exercise regimens may help achieve this goal or even improve glucose control without weight loss. Due to the heterogeneity of the disease individualized treatment must be used to improve status of patients with the various metabolic defects of Type II diabetes.     

Dietary fructose: implications for dysregulation of energy homeostasis and lipid/carbohydrate metabolism

Fructose intake and the prevalence of obesity have both increased over the past two to three decades. Compared with glucose, the hepatic metabolism of fructose favors lipogenesis, which may contribute to hyperlipidemia and obesity. Fructose does not increase insulin and leptin or suppress ghrelin, which suggests an endocrine mechanism by which it induces a positive energy balance. This review examines the available data on the effects of dietary fructose on energy homeostasis and lipid/carbohydrate metabolism. Recent publications, studies in human subjects, and areas in which additional research is needed are emphasized.     

Dietary hydrogenated soybean oil affects lipid and vitamin E metabolism in rats

Fatty acids containing stearic acid, which are found in hydrogenated fat, may have a detrimental effect on the cholesterol and triacylglycerol (TAG) content of plasma lipoproteins, and on the absorption of fatty acids and fat-soluble vitamins. The aim of our study was to examine the tissue concentration of lipids and vitamins A and E after feeding a hydrogenated soybean oil (HSO) diet to rats. Twenty male Sprague-Dawley rats were randomly divided into two groups, fed on coconut oil (control) and HSO, respectively in amounts corresponding to 15% of the total feed. Plasma total cholesterol, VLDL- and LDL-cholesterol, lipid peroxidation and daily excretion of the TAG and cholesterol in feces were higher in the HSO than in the control group. TAG values in plasma and liver, and HDL-cholesterol levels in plasma were lower in the HSO than in the control group. The same was true for phospholipids in plasma and for saturated fatty acids, mono- and polyunsaturated fatty acids levels in the liver and vitamin E in plasma, LDL and adipose tissue. The results of this study provide new evidence concerning the effect of dietary hydrogenated fat on lipid, TAG and vitamin E status, which are important for maintenance of good health. Consumption of dietary HSO may be associated with cardiovascular disease.     

Dietary effect of pomegranate seed oil on immune function and lipid metabolism in mice

OBJECTIVES: We evaluated the effects of dietary pomegranate seed oil (PSO), which contains high levels of punicic acid (9c, 11t, 13c-octadecatrienoic acid), on immune function and lipid metabolism in C57BL/6N mice. METHODS: Mice were fed experimental diets containing 0%, 0.12%, or 1.2% PSO for 3 wk. RESULTS: No significant differences were observed between growth patterns of the experimental groups. Splenocytes isolated from mice fed 0.12% or 1.2% PSO produced larger amounts of immunoglobulins G and M but not immunoglobulin A irrespective of stimulation with or without phorbol 12-myristate 13-acetate and the calcium ionophore A23187. Dietary PSO did not affect the percentages of B cells or CD4-positive or CD8-positive T cells in splenocytes. Levels of interleukin-4, interferon-gamma, and tumor necrosis factor-alpha production from splenocytes were comparable among all dietary groups. Analysis of serum lipid parameters showed significant increases in serum triacylglycerol and phospholipid levels but not in total cholesterol in the PSO groups. Serum, liver, epididymal, and perirenal adipose punicic acid levels were high with increases in dietary PSO level. However, punicic acid was not detected in splenocytes for any dietary group. Interestingly, 9c, 11t-conjugated linoleic acid level could be detected in serum, liver, and adipose tissues in mice fed the 0.12% or 1.2% PSO diet. CONCLUSIONS: These results suggest that PSO may enhance B-cell function in vivo.     

Dietary carbohydrate: relationship to cardiovascular disease and disorders of carbohydrate metabolism

The nature of carbohydrate is of considerable importance when recommending diets intended to reduce the risk of type II diabetes and cardiovascular disease and in the treatment of patients who already have established diseases. Intact fruits, vegetables, legumes and wholegrains are the most appropriate sources of carbohydrate. Most are rich in nonstarch polysaccharides (NSPs) (dietary fibre) and other potentially cardioprotective components. Many of these foods, especially those that are high in dietary fibre, will reduce total and low-density lipoprotein cholesterol and help to improve glycaemic control in those with diabetes. There is no good long-term evidence of benefit when NSPs or other components of wholegrains, fruits, vegetables and legumes are added to functional and manufactured foods. Frequent consumption of low glycaemic index foods has been reported to confer similar benefits, but it is not clear whether such benefits are independent of the dietary fibre content of these foods or the fact that low glycaemic index foods tend to have intact plant cell walls. Furthermore, it is uncertain whether functional and manufactured foods with a low glycaemic index confer the same long-term benefits as low glycaemic index plant-based foods. A wide range of carbohydrate intake is acceptable, provided the nature of carbohydrate is appropriate. Failure to emphasize the need for carbohydrate to be derived principally from wholegrain cereals, fruits, vegetables and legumes may result in increased lipoprotein-mediated risk of cardiovascular disease, especially in overweight and obese individuals who are insulin resistant.     

The effects of diet differing in fat, carbohydrate, and fiber on carbohydrate and lipid metabolism in type II diabetes

This study was designed to determine the effects of varying the proportions of carbohydrate, fiber, and fat on metabolic control in Type II diabetes. Ten men, aged 50 to 69 years, with Type II diabetes participated. Four isocaloric diets were consumed for 2 weeks each, with a break of 6 to 14 weeks between diets to ensure no carryover effects. Two of the diets were high in carbohydrate (63% to 65% energy) and low in fat (10% to 12% energy) but differed in their fiber contents (20 vs. 45 gm/day). The other two diets were low in carbohydrate (23% to 27% energy) with either a low or a high fat content (15% vs. 55% energy) and a high or normal protein content (62% vs. 18% energy). The composition of the subjects' usual diets in the week before each of the experimental diets did not vary significantly: carbohydrate 47% to 50% energy, protein 22% to 25% energy, fat 27% to 31% energy, and fiber 24 to 25 gm/day. A 75-gm oral glucose tolerance test and a 12-hour metabolic profile in response to 3 meals typical of the particular diet were conducted before and at the conclusion of each 2-week dietary period. The most significant improvements in metabolic control (as assessed by the effects of the diets on fasting glucose and on lipids, and on the glucose and insulin responses to oral glucose and the mixed meals) were obtained with the high-fiber, high-carbohydrate, low-fat diet and with the low-carbohydrate, high-protein, low-fat diet. Metabolic control was not significantly affected by the low-fiber, high-carbohydrate, low-fat diet, but it deteriorated significantly on the low-carbohydrate, high-fat diet. The results of this study confirmed the importance of high fiber and low fat in improving metabolic control in Type II diabetes. In conclusion, if high-carbohydrate, low-fat diets are to be recommended to patients with diabetes, it is essential that the type of carbohydrate recommended be unrefined and high in fiber.     

Effect of exercise on lipid metabolism of rats fed high carbohydrate diets.

Two experiments were conducted to determine whether high carbohydrate diets or exercise would have a greater influence on certain parameters of lipid metabolism. Male Fischer rats were used in both experiments, separated into exercise and sedentary groups, and fed either a high sucrose (63%) or a high starch (63%) diet. There were no differences in body weight or food consumption between the two diets. Exercise resulted in a highly significant increase in food consumption in both experiments. Rats fed sucrose had a higher serum cholesterol value than rats fed starch. Diet did not influence serum triglycerides but the rats on excercise had significantly lower serum triglycerides than the sedentary rats. Liver weight was significantly larger in rats fed sucrose. Sucrose caused an increase in the activity of both glucose-6-phosphate dehydrogenase and malic enzyme activities in liver tissue, whereas exercise caused an increase in the activity of these enzymes in adipose tissue.     

高糖高脂饲料对Wistar大鼠生长和糖脂代谢的影响

目的观察高糖高脂饲料对Wistar大鼠生长及糖脂代谢的影响。方法雄性Wistar大鼠20只,按体重和空腹血糖随机分为2组(n=10):对照组和实验组,分别以普通饲料和高糖高脂饲料喂养6周,观察大鼠的生长曲线、食物利用率,测定大鼠的糖脂代谢指标。结果喂养6周后,实验组大鼠的体重、食物利用率、内脏脂肪占体重百分比、血清总胆固醇和低密度脂蛋白胆固醇均显著高于对照组(P<0.05),血清高密度脂蛋白胆固醇显著低于对照组(P<0.01)。两组的空腹血糖(FPG)无显著差异。实验组大鼠的糖耐量降低,葡萄糖曲线下面积显著高于对照组。结论正常血糖状态下,高糖高脂饲料可引起Wistar大鼠中心型积聚的体脂增加,血清总胆固醇增加,导致葡萄糖耐量能力减退,为2型糖尿病进程中的重要危险因素。     

Dietary selenium affects homocysteine metabolism differently in Fisher-344 rats and CD-1 mice

In our previous work with rats, plasma and tissue homocysteine concentrations were decreased by selenium deprivation. The purpose of this study was to follow up and expand on that work by determining the effects of selenium status (deficient, adequate, and supranutritional) on several aspects of homocysteine metabolism involving methionine recycling and transsulfuration. A 2nd objective was to determine whether there are differences in how selenium status affects homocysteine metabolism in rats and mice. Male weanling Fischer-344 rats and male weanling CD-1 mice were fed diets containing 0, 0.2, or 2.0 microg selenium (as sodium selenite)/g for 72 d or 60 d, respectively. Plasma homocysteine and cysteine were significantly decreased by feeding rats or mice the selenium-deficient diet compared with feeding adequate or supranutritional selenium. On the other hand, plasma glutathione was increased by selenium deficiency only in rats. Also, the specific activities of liver betaine homocysteine methyltransferase and glycine N-methyltransferase were decreased by selenium deficiency in rats, but were unaffected by selenium status in mice. Real-time RT-PCR was used to determine the expression of the subunits of glutamate-cysteine ligase, which catalyzes the rate-limiting step in glutathione biosynthesis. The expression of Gclc, the catalytic subunit of glutamate-cysteine ligase, was upregulated by selenium deprivation in both rat and mouse liver. Gclm, the modifier subunit of glutamate-cysteine ligase, was downregulated in rats fed 2 microg Se/g compared with rats fed adequate or deficient selenium. Based on these findings, it is evident that selenium deficiency has different outcomes in mice and rats. These variables are all related to methionine/methyl metabolism. Although only one strain of rat was compared with one strain of mouse, this work suggests that differences between species may prove vital in determining which animal model is used in studies of selenium deficiency or in studies that are designed to ascertain chemopreventive mechanisms of selenium.     

Dietary palatinose and oleic acid ameliorate disorders of glucose and lipid metabolism in Zucker fatty rats

Excessive dietary intake of carbohydrates and fats has been linked to the development of obesity. However, the mechanism by which these dietary factors interact to bring about metabolic changes has not been elucidated. We examined the combined effects of different types of dietary carbohydrates and fats on the etiology of obesity and its complications in the Zucker fatty (fa/fa) rat, a model of obesity. Specifically, these rats were fed an isocaloric diet containing various combinations of carbohydrates [palatinose (P), an insulin-sparing sucrose analogue, and sucrose (S)] and fatty acids [oleic acid (O) and linoleic acid (L)]. After 8 wk, palatinose feeding (PO and PL) led to significant reductions in visceral fat mass, adipocyte cell size, hyperglycemia, and hyperlipidemia compared with sucrose feeding (SO and SL); pancreatic islet hypertrophy was also prevented by palatinose feeding. Linoleic-acid-fed rats (PL and SL) exhibited reduced insulin-immunoreactive staining of the pancreatic islets, enhanced macrophage infiltration in adipose tissue, and an elevated plasma tumor necrosis factor-alpha concentration when compared with oleic-acid-fed rats (PO and SO). Furthermore, sucrose and linoleic acid synergistically increased the expression of genes involved in hepatic gluconeogenesis and lipogenesis [sterol regulatory-element binding protein (SREBP)-1c and SREBP-2]. In conclusion, a diet containing palatinose and oleic acid may prevent diet-induced metabolic abnormalities. The combination of palatinose and oleic acid holds promise for a new approach to preventing and treating obesity and its complications.     

Favorable effects of egg white protein on lipid metabolism in rats and mice

Egg is a cholesterol-rich food and has a strong hyper-cholesterolemic action. However, all the cholesterol is in egg yolk and egg white is cholesterol-free. The effect of egg white protein and its hydrolysates on the serum lipids were compared with casein and soybean protein in rats and mice. The animals were given 30% casein diet (Ca group) or diets of 15% casein plus 15% soybean protein isolate (SPI group), egg white protein (EW group) or egg white protein hydrolysates (EW-P group) for 3 (rats) or 2 (mice) weeks. Food intake and growth were very similar among the different dietary groups. Hypocholesterolemic effect was observed in SP, EW and EW-P groups in rats and EW group in mice. Prevention of the reduction of HDL-cholesterol was found in EW and EW-P groups in rats and EW-P group in mice. The result suggests the possibility of the use of egg white for the prevention and treatment of hyper-cholesteremia.     

Long-term effects of Depo-Provera on carbohydrate and lipid metabolism

Long-term effects of injection Depo-Provera (depo-medroxyprogesterone acetate) on carbohydrate and lipid metabolism were studied in 157 women who were treated continuously for a mean duration of 43.3 months. The patients were matched with 162 controls for race, age, parity and height. Glucose tolerance was impaired with higher intolerance at longer duration. Glucose areas were significantly higher at 48 and 60 months of injection. Insulin levels were also significantly decreased at 30 minutes and increased at 150 minutes but the area was normal. Triglycerides were initially decreased, being significant at 36 months (p less than 0.001) and returned to normal at 60 months while cholesterols were significantly higher at 24 and 36 months (p less than 0.05) and 60 months (p less than 0.001). In view of these findings, Depo-Provera may have an advantage over oral pills on a short term basis as there are less alterations in carbohydrate and lipid metabolism.     

L-阿拉伯糖对2型糖尿病大鼠糖脂代谢的影响

目的探讨L-阿拉伯糖对2型糖尿病模型大鼠血糖、血脂、脏器及胰岛的影响。方法采用雄性Wistar大鼠高糖高脂饲料喂养8周后,按25mg/kgbw的剂量一次性腹腔注射链脲佐菌素建立2型糖尿病动物模型,按L-阿拉伯糖低剂量(50mg/kgbw)、中剂量(150mg/kgbw)及高剂量(500mg/kgbw)进行灌胃,以阿卡波糖(20mg/kgbw)作为阳性对照,所用L-阿拉伯糖及阿卡波糖均配制于糊精(0.36g/ml)与蔗糖(0.04g/ml)的悬浮液中,自由进食进水。给药4周后进行口服葡萄糖耐量试验,处死后对大鼠肝脏、附睾脂肪及盲肠进行称重,腹主动脉取血测定TC、TG、血糖及胰岛素水平,通过免疫组织化学切片对胰岛β细胞损伤程度进行评价。结果与模型组对比,低、中、高剂量的L-阿拉伯糖干预对糖尿病大鼠的血糖应答产生了显著影响,30、60和120min血糖值及AUC均显著低于模型对照组(P<0.05),其中以中剂量效果最为显著(P<0.01)。L-阿拉伯糖的干预对糖尿病大鼠胰岛素敏感性的改善未见显著,但增加了盲肠重量,对胰岛β细胞也呈现出保护作用。本研究中L-阿拉伯糖的干预对于血脂和血胆固醇的影响较小。结论 L-阿拉伯糖的中长期干预能够改善2型糖尿病大鼠的糖耐量,这种作用可能与L-阿拉伯糖对食物消化酶的抑制及对胰岛β细胞的保护作用相关。