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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

These studies were designed to determine whether genetically and experimentally induced hypertriglyceridemia were correlated with hyperlipogenesis, and whether inhibiting fatty acid synthesis would reduce serum triglyceride levels. Hypertrigylceridemia, resulting from genetic obesity in Zucker rats and fructose feeding or Triton administration to Charles River rats, was examined in relation to in vivo rates of heatic fatty acid synthesis, and the influence of (--)-hydroxycitrate (a potent competitive inhibitor of ATP citrate lyase) on serum triglyceride levels and lipogenesis was determined. Zucker obese rats demonstrated significantly increased rates of fatty acid synthesis and levels of serum triglycerides compared to their lean litter mates; lipogenic rates and circulating triglycerides were reduced markedly by the oral administration of (--)-hydroxycitrate. Fructose administered in the diet or drinking water induced a hypertriglyceridemia which was associated with a marked increase in hepatic lipogenesis, and (--)-hydroxycitrate reduced significantly both parameters. In contrast to the significant role that increased rates of lipogenesis apparently played in the development of hypertriglyceridemia in the Zucker rat and fructose-fed rat, Triton given intravenously produced a marked rise in serum triglycerides which could not be accounted for, to an appreciate extent, by increased rates of fatty acid synthesis. (--)-Hydroxycitrate reduced serum triglyceride levels and hepatic lipogenic rates equivalently in the Triton-treated and nontreated rats.
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PMID:Metabolic regulation as a control for lipid disorders. II. Influence of (--)-hydroxycitrate on genetically and experimentally induced hypertriglyceridemia in the rat. 85 44

It is now recognized that dietary carbohydrate components influence the prevalence and severity of common degenerative diseases such as dental problems, diabetes, heart disease and obesity. Fructose and sucrose have been evaluated and compared to glucose using glucose tolerance tests, but few such comparisons have been performed for a "natural" sugar source such as honey. In this study, 33 upper trimester chiropractic students volunteered for oral glucose tolerance testing comparing sucrose, fructose and honey during successive weeks. A 75-gm carbohydrate load in 250 ml of water was ingested and blood sugar readings were taken at 0, 30, 60, 90, 120 and 240 minutes. Fructose showed minimal changes in blood sugar levels, consistent with other studies. Sucrose gave higher blood sugar readings than honey at every measurement, producing significantly (p less than .05) greater glucose intolerance. Honey provided the fewest subjective symptoms of discomfort. Given that honey has a gentler effect on blood sugar levels on a per gram basis, and tastes sweeter than sucrose so that fewer grams would be consumed, it would seem prudent to recommend honey over sucrose.
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PMID:Differential effects of honey, sucrose, and fructose on blood sugar levels. 200 97

Ingestion of nutrients increases energy expenditure above basal metabolic rate. Thermogenesis of carbohydrate comprises two distinct components: an obligatory component, which corresponds to the energy cost of carbohydrate absorption, processing, and storage; and a facultative component, which appears to be related with a carbohydrate-induced stimulation of the sympathetic nervous system, and can be inhibited by beta-adrenergic antagonists. Fructose ingestion induces a greater thermogenesis than does glucose. This can be explained by the hydrolysis of 3.5-4.5 mol ATP/mol fructose stored as glycogen, vs 2.5 mol ATP/mol glucose stored. Therefore the large thermogenesis of fructose corresponds essentially to an increase in obligatory thermogenesis. Obese individuals and obese patients with non-insulin-dependent diabetes mellitus commonly have a decrease in glucose-induced thermogenesis. These individuals in contrast display a normal thermogenesis after ingestion of fructose. This may be explained by the fact that the initial hepatic fructose metabolism is independent of insulin. This observation indicates that insulin resistance is likely to play an important role in the decreased glucose-induced thermogenesis of these individuals.
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PMID:Fructose and dietary thermogenesis. 821 8

The JCR:LA-corpulent rat is a strain exhibiting marked obesity and metabolic derangements characterized by hyperlipidemia due to hypersecretion of very-low-density lipoprotein (VLDL) and severe insulin resistance. The corpulent male rats spontaneously develop atherosclerosis and ischemic myocardial lesions. Male corpulent rats were treated with acarbose in the presence and absence of sugar-supplemented diets. The acarbose-treated rats had lower body weights at 3 months of age with unaltered food consumption, and a similar effect was seen with a high-fructose diet. Fasting insulin concentrations were decreased significantly in acarbose-treated animals at both 3 and 9 months of age, and the rate of plasma glucose disappearance increased at 3 months of age. Acarbose treatment did not affect whole-serum triglyceride concentrations, but there were modest decreases in cholesterol levels. Sugar-supplemented diets caused no significant changes in insulin or glucose concentrations, and caused small increases in nonesterified cholesterol only. Fructose- but not sucrose-supplemented diets were associated with a significantly decreased frequency of old scarred myocardial lesions. The frequency of occurrence of such lesions was also decreased by acarbose treatment. This effect of acarbose treatment may reflect improvement in insulin and glucose metabolism in treated rats. The decrease in myocardial lesions in fructose-fed rats may be secondary to increased carbohydrate metabolism via the pathways leading from fructose to triglyceride.
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PMID:Beneficial effects of acarbose in the atherosclerosis-prone JCR:LA-corpulent rat. 847 19

Frequent coexistence of insulin resistance, central obesity, and hypertriglyceridemia in the same individual suggests an underlying common pathogenesis. Insulin resistance and hypertriglyceridemia can be induced by carbohydrate feeding in rats. Golden Syrian hamsters are believed to be resistant to the metabolic effects of dietary carbohydrates. We investigated the effects of diets containing 60% fructose or sucrose on glucose and lipid metabolism in hamsters, both in the fasting state and during an intravenous glucose tolerance test. Fructose caused obesity (weight after treatment: 131 +/- 7 gm in the control group, 155 +/- 5 gm in the fructose group, 136 +/- 7 gm in sucrose group, p < 0.04). Fructose also reduced glucose disappearance rate (KG: 2.69% +/- 0.39% in the control group, 1.45% +/- 0.18% in the fructose group, p < 0.02). Sucrose caused a marginal decrease in glucose disappearance (KG: 1.93% +/- 0.21%, p = 0.08 vs the control group). Only fructose feeding increased fasting plasma nonesterified fatty acids (0.645 +/- 0.087 mEq/L in the control group, 1.035 +/- 0.083 mEq/L in the fructose group, 0.606 +/- 0.061 mEq/L in the sucrose group, p < 0.002), plasma triglycerides (84 +/- 6 mg/dl in the control group, 270 +/- 65 mg/dl in the fructose group, 94 +/- 16 mg/dl in the sucrose group, p < 0.0002), and liver triglycerides (1.88 +/- 0.38 mg/gm liver weight in the control group, 2.35 =/- 0.24 mg/gm in the fructose group, 1.41 +/- 0.13 mg/gm in the sucrose group, p < 0.04). Previous studies in the rat have suggested that dietary carbohydrates induce insulin resistance by increasing plasma nonesterified fatty acids and triglycerides, which are preferentially used by the muscles. The present report shows that sucrose also can cause some decrease in glucose disappearance in the hamster without causing hypertriglyceridemia or increasing plasma nonesterified fatty acids. Thus other mechanisms may also contribute to the insulin resistance in the hamster. These findings suggest that hamsters provide a good model for investigation of hormonal and nutritional regulation of glucose and lipid metabolism.
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PMID:Effects of dietary carbohydrates on glucose and lipid metabolism in golden Syrian hamsters. 876 17

Experiments were conducted to investigate the effects of activation of cardiopulmonary vagal afferent nerve endings by acute saline volume expansion on sympathetic efferent renal nerve activity in anaesthetised fat-fed and fructose-fed Wistar rats. Four weeks of fat feeding caused obesity in the Wistar rats which was associated with a mild elevation in blood pressure (118 +/- 4 mmHg vs. 105 +/- 1 mmHg in the lean control rats, P < 0.05). Fructose feeding in Wistar rats for 4 weeks also elicited an elevation of blood pressure (113 +/- 4 mmHg, P < 0.05) and plasma glucose levels (6.3 +/- 0.3 mmol/l vs. 4.0 +/- 0.3 mmol/l lean control rats, P < 0.01). The fat-fed rats displayed a higher basal renal sympathetic nerve activity (RSNA) value when compared with the lean rats (3.9 +/- 0.4 mV/s vs. 2.8 +/- 0.4 mV/s, P < 0.05) whereas the RSNA levels were similar in all the other rat groups. The power spectral analysis of RSNA showed the basal values of percentage power at heart rate frequency were significantly higher in Wistars fed ad lib (P < 0.01), rats fed on fructose for 2 or 4 weeks (P < 0.01 and P < 0.05, respectively) and fat-fed rats (P < 0.01) when compared to the lean diet-controlled rats. Acute volume expansion (10% body wt) over 40 min caused efferent renal sympatho-inhibition in all the animal groups. The pattern and magnitude of response in MAP, RSNA, and power spectral analysis parameters to the volume expansion were similar in the lean control rats, the Wistar and fructose fed rats but was greater in the fat-fed rats (P < 0.05) as compared to the lean control rat. The profile of the reduction in percentage power at heart rate frequency to volume expansion was greater (P < 0.05) in the fat-fed rat than in the lean control rats. The present data demonstrates that the reflex efferent renal sympatho-inhibition to volume expansion was impaired in the diet-induced obese rat but not in the fructose fed rats. This suggests that a defect in the neuro-humoral regulation of kidney control of extracellular fluid volume is present which may contribute to the mild hypertension in the obese rat.
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PMID:Effect of acute saline volume loading on renal sympathetic nerve activity in anaesthetised fructose-fed and fat-fed rats. 993 70

This review explores whether fructose consumption might be a contributing factor to the development of obesity and the accompanying metabolic abnormalities observed in the insulin resistance syndrome. The per capita disappearance data for fructose from the combined consumption of sucrose and high-fructose corn syrup have increased by 26%, from 64 g/d in 1970 to 81 g/d in 1997. Both plasma insulin and leptin act in the central nervous system in the long-term regulation of energy homeostasis. Because fructose does not stimulate insulin secretion from pancreatic beta cells, the consumption of foods and beverages containing fructose produces smaller postprandial insulin excursions than does consumption of glucose-containing carbohydrate. Because leptin production is regulated by insulin responses to meals, fructose consumption also reduces circulating leptin concentrations. The combined effects of lowered circulating leptin and insulin in individuals who consume diets that are high in dietary fructose could therefore increase the likelihood of weight gain and its associated metabolic sequelae. In addition, fructose, compared with glucose, is preferentially metabolized to lipid in the liver. Fructose consumption induces insulin resistance, impaired glucose tolerance, hyperinsulinemia, hypertriacylglycerolemia, and hypertension in animal models. The data in humans are less clear. Although there are existing data on the metabolic and endocrine effects of dietary fructose that suggest that increased consumption of fructose may be detrimental in terms of body weight and adiposity and the metabolic indexes associated with the insulin resistance syndrome, much more research is needed to fully understand the metabolic effect of dietary fructose in humans.
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PMID:Fructose, weight gain, and the insulin resistance syndrome. 1452 42

Fructose is a major dietary sugar, which is elevated in the serum of diabetic humans, and is associated with metabolic syndromes important in the pathogenesis of diabetic complications. The facilitative fructose transporter, GLUT5, is expressed in insulin-sensitive tissues (skeletal muscle and adipocytes) of humans and rodents, where it mediates the uptake of substantial quantities of dietary fructose, but little is known about its regulation. We found that GLUT5 abundance and activity were compromised severely during obesity and insulin resistance in Zucker rat adipocytes. Adipocytes from young obese (fa/fa), highly insulin-responsive Zucker rats contained considerably more plasma membrane GLUT5 than those from their lean counterparts (1.8-fold per microgram membrane protein), and consequently exhibited higher fructose transport (fivefold) and metabolism (threefold) rates. Lactate production was the preferred route for fructose metabolism in these cells. As the rats aged and become more obese and insulin-resistant, adipocyte GLUT5 surface density (12-fold) and fructose transport (10-fold) and utilisation rates (threefold) fell markedly. The GLUT5 loss was more dramatic in adipocytes from obese animals, which developed a more marked insulin resistance than lean counterparts. The decline of GLUT5 levels in adipocytes from older, obese animals was not a generalised effect, and was not observed in kidney, nor was this expression pattern shared by the alpha1 subunit of the Na+/K+ ATPase. Our findings suggest that plasma membrane GLUT5 levels and thus fructose utilisation rates in adipocytes are dependent upon cellular insulin sensitivity, inferring a possible role for GLUT5 in the elevated circulating fructose observed during diabetes, and associated pathological complications.
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PMID:Fructose transport and metabolism in adipose tissue of Zucker rats: diminished GLUT5 activity during obesity and insulin resistance. 1536 82

With the prevalence of obesity increasing in the U.S. and elsewhere, the place of carbohydrates in the diet has recently been under closer examination. This has led to the development of methods for analyzing the effects of dietary carbohydrate. Primary among these methods is the glycemic index, a measure of a food's effect on blood glucose levels, which was initially designed as a method for determining suitable carbohydrates for people with diabetes. However, the glycemic index does not address other metabolic issues related to excess sugar consumption. Prominent among these issues is the use of low glycemic index sweeteners, particularly fructose, which is increasingly present in processed food. Fructose is associated with increased adiposity, which may result from its effects on hormones associated with satiety. Other methods of determining "good" carbohydrates have also been developed. The common theme among them is increased nonstarchy vegetables and higher-fiber legumes.
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PMID:Carbohydrates and increases in obesity: does the type of carbohydrate make a difference? 1560 60

Obesity and type 2 diabetes are occurring at epidemic rates in the United States and many parts of the world. The "obesity epidemic" appears to have emerged largely from changes in our diet and reduced physical activity. An important but not well-appreciated dietary change has been the substantial increase in the amount of dietary fructose consumption from high intake of sucrose and high fructose corn syrup, a common sweetener used in the food industry. A high flux of fructose to the liver, the main organ capable of metabolizing this simple carbohydrate, perturbs glucose metabolism and glucose uptake pathways, and leads to a significantly enhanced rate of de novo lipogenesis and triglyceride (TG) synthesis, driven by the high flux of glycerol and acyl portions of TG molecules from fructose catabolism. These metabolic disturbances appear to underlie the induction of insulin resistance commonly observed with high fructose feeding in both humans and animal models. Fructose-induced insulin resistant states are commonly characterized by a profound metabolic dyslipidemia, which appears to result from hepatic and intestinal overproduction of atherogenic lipoprotein particles. Thus, emerging evidence from recent epidemiological and biochemical studies clearly suggests that the high dietary intake of fructose has rapidly become an important causative factor in the development of the metabolic syndrome. There is an urgent need for increased public awareness of the risks associated with high fructose consumption and greater efforts should be made to curb the supplementation of packaged foods with high fructose additives. The present review will discuss the trends in fructose consumption, the metabolic consequences of increased fructose intake, and the molecular mechanisms leading to fructose-induced lipogenesis, insulin resistance and metabolic dyslipidemia.
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PMID:Fructose, insulin resistance, and metabolic dyslipidemia. 1572 2


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