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

Authors reviews--upon literature data--the metabolism of carbohydrates, with special regard to lipogenesis, which is of less importance and has no role in obesity. Out of the plasma lipids, in the case of extreme sugar consumption, only the level of triglicerides shows increase. Sugar is one but not the only factor caries. Sugar promotes the learning and remembering function of the brain and possibly, affects behaviour, too. Oligosaccharides may contribute to the favourable changes in the intestinal microflora. Carbohydrates and within them, sugars, play no unfavourable role in the development of diabetes mellitus, obesity, cardiovascular disease, when nutrition is well balanced.
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PMID:[Physiological role of dietary carbohydrates in diet of hungarian population. Epidemiological study]. 982 67

Insulin resistance is a metabolic syndrome commonly seen in obesity. Leptin, the obese gene product, plays a role in the regulation of cardiac function. Elevated leptin levels have been demonstrated under insulin-resistant states such as obesity and hypertension, although their role in cardiac dysfunction is unknown. This study was designed to determine the impact of prediabetic insulin resistance on leptin levels and leptin-induced cardiac contractile response. Whole-body insulin resistance was generated with a 10-week dietary sucrose feeding. Contractile and intracellular Ca(2+) properties were evaluated in ventricular myocytes using an IonOptix system. The contractile indices analyzed included peak shortening (PS), time-to-PS (TPS), time-to-90% relengthening (TR(90)), maximal velocity of shortening/relengthening (+/-dL/dt), fura-fluorescence intensity change (deltaFFI) and decay rate (tau). Sucrose-fed rats displayed significantly elevated body weight and plasma leptin levels, depressed PS, +/-dL/dt, shortened TPS, prolonged TR(90) and tau, as well as reduced deltaFFI compared to the starch-fed control group. Leptin (1-1000 nM) elicited a concentration-dependent depression of PS and deltaFFI in myocytes from both starch and sucrose groups. Leptin-induced contractile depression was abolished by the nitric oxide synthase inhibitor Nomega-nitro-L-arginine methyle ester, elevation of the extracellular Ca(2+) concentration, the Janus activated kinase 2 inhibitor AG-490 or the mitogen activated protein kinase inhibitor SB203580 in myocytes from both sucrose and starch groups. Moreover, AG-490 and SB203580 unmasked a positive response of PS in myocytes from both groups. These data indicate that insulin resistance directly induces hyperleptinemia and cardiac contractile dysfunction, without affecting leptin-mediated cardiac contractile function at the myocyte level.
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PMID:Insulin resistance induces hyperleptinemia, cardiac contractile dysfunction but not cardiac leptin resistance in ventricular myocytes. 1451 67

Sucrose- and fructose-enriched diets produce hepatic insulin resistance in rats independently of obesity. In humans, fructose infusion results in impaired insulin regulation of glucose production. The aim of the present study was to identify intrahepatic mediators of sucrose- and fructose-induced hepatic insulin resistance. In study 1, male rats were fed a control diet (STD, 68% of energy from corn starch, 12% from corn oil) or a sucrose-enriched diet (HSD, 68% sucrose, 12% corn oil) for 1, 2, or 5 wk. HSD produced hepatic insulin resistance at all time points. Hepatic protein tyrosine phosphatase 1B protein levels and activity were increased at 5 wk only, whereas c-jun NH(2)-terminal kinase (JNK) activity was increased at all time points. Normalization of JNK activity in hepatocytes isolated from HSD rats improved insulin-stimulated tyrosine phosphorylation of insulin receptor substrate (IRS) proteins and insulin suppression of glucose release. In study 2, male rats were provided STD for 1 wk and then were either fasted or fasted and refed either STD or HSD for 3 or 6 h. Rats refed HSD were characterized by increased hepatic JNK activity and phosphorylation of IRS1 on Ser(307) after 6 h only. In study 3, hyperglycemic, hyperinsulinemic pancreatic clamps were performed for 3 or 6 h in the presence or absence of low or high intraportal fructose infusions. High intraportal fructose infusions, which increased portal vein fructose concentration to approximately 1 mM, increased hepatic JNK activity and phosphorylation of IRS1 on Ser(307) at 6 h only. These data suggest that sucrose- and fructose-induced hepatic insulin resistance are mediated, in part, via activation of JNK activity. Thus high rates of fructose metabolism in the liver appear to acutely activate stress pathways.
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PMID:Hepatospecific effects of fructose on c-jun NH2-terminal kinase: implications for hepatic insulin resistance. 1519 36

Overfeeding of some waterfowl species results in obesity, which is mainly characterized by a dramatic hepatic steatosis induced by strong accumulation of lipids synthesized from dietary glucose in the liver. In mammals, fructose is known to be able to raise plasma triacylglycerol concentrations significantly; consequently, this may induce obesity. The aim of this study was to assess the effect of partial replacement of dietary glucose provided by corn starch with fructose on metabolism and fatty liver production in the Mule ducks. On the basis of 9.5 kg maize (132,920 kJ) given twice a day for 14 days, a supplementation of 9,800 kJ was provided in form of glucose, sucrose or high fructose corn syrup (HFCS: 50 % glucose, 42 % fructose and 8 % other saccharides). Fatty liver weight in ducks fed with glucose supplementation was 499 +/- 21 g. Sucrose or HFCS supplementation brought about a significant increase in liver weight (+ 18.7 % and + 16.3 % vs. glucose supplementation respectively, p < 0.05). These results suggest that the dietary fructose favors the liver steatosis by increasing hepatic lipogenesis. Postprandial plasma insulin concentrations were similar in ducks fed diets with or without fructose, suggesting that the effect of fructose on liver steatosis is not mediated by insulin.
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PMID:Effects of dietary fructose on liver steatosis in overfed mule ducks. 1570 36

Current scientific evidence indicates that dietary fat plays a role in weight loss and maintenance. Meta-analyses of intervention trials find that fat-reduced diets cause a 3-4-kg larger weight loss than normal-fat diets. A 10% reduction in dietary fat can cause a 4-5-kg weight loss in individuals with initial body mass index of 30 kg m (-2). Short-term trials show that nonfat dietary components are equally important. Sugar-sweetened beverages promote weight gain, and replacement of energy from fat by sugar-sweetened beverages is counterproductive in diets aimed at weight loss. Protein has been shown to be more satiating than carbohydrate, and fat-reduced diets with a high protein content (20-25% of energy) may increase weight loss significantly. There is little evidence that low-glycemic index foods facilitate weight control. Evidence linking certain fatty acids to body fatness is weak. Monounsaturated fatty acids may even be more fattening than polyunsaturated and saturated fats. No ad libitum dietary intervention study has shown that a normal-fat, high-monounsaturated fatty acid diet is comparable to a low-fat diet in preventing weight gain. Current evidence indicates that the best diet for prevention of weight gain, obesity, type 2 diabetes, and cardiovascular disease is low in fat and sugar-rich beverages and high in carbohydrates, fiber, grains, and protein.
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PMID:The role of dietary fat in obesity. 1596 79

Sucrose is more lipogenic than starch, and the extreme ingestion of sucrose induces adiposity and obesity. The aim of this study was to examine the effect of the eucalyptus (Eucalyptus globulus) leaf extract (ELE) on adiposity due to dietary sucrose in rats. In addition, in this study, the effect of ELE on intestinal fructose absorption was also examined. Rats were fed a high-sucrose diet (75 % in calorie base) with or without ELE (10 g/kg diet) for 5 weeks. Body weight was lower in the rats receiving ELE than in the controls (342 (sd 37.9) v. 392 (sd 26.0) g (n 7); P<0.05). Furthermore, ELE resulted in decreases in the triacylglycerol concentrations in the plasma (1.44 (sd 0.448) v. 2.79 (sd 0.677) mmol/l (n 7); P<0.05) and liver (19.1 (sd 5.07) v. 44.1 (sd 16.28) micromol/g (n 7); P<0.05). In contrast, ELE did not show any significant effects in the rats fed a starch diet. When rats were orally given ELE 10 min before fructose administration, the intestinal fructose absorption, which was examined by measuring the elevated concentration of fructose in the portal vein at 30 min after the fructose administration, was significantly inhibited in a dose-dependent manner. Furthermore, in rats fed a high-fructose diet, the plasma and hepatic triacylglycerol concentrations were significantly decreased by ELE. These results indicate that ELE, which inhibits the intestinal fructose absorption, can suppress adiposity in rats that ingest large amounts of sucrose or fructose.
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PMID:Eucalyptus leaf extract inhibits intestinal fructose absorption, and suppresses adiposity due to dietary sucrose in rats. 1602 67

Sucrose polyester, a fat substitute, has shown promise in reducing blood cholesterol and body weight of obese individuals. Effects of this compound in the Zucker rat, a genetic model of obesity, are unknown. Thus, we examined food intake, body weight, body composition, and several metabolic parameters in sera of lean and obese female Zucker rats. Eight-week-old lean and obese animals were given a choice between a control diet (15% corn oil) and fat substitute diet (5% corn oil and 10% sucrose polyester) for 2 days. Next, one-half of the lean and obese groups received control diet; the remaining lean and obese rats received fat substitute diet for 18 days. Cumulative food intake was depressed in fat substitute groups relative to control-fed animals; however, this effect was more predominant in obese animals. Obese rats consuming fat substitute diet (O-FS) gained less weight as compared to obese control-fed animals (O-C). Lean rats given fat substitute (L-FS) did not have significantly different body weights as compared to the L-C group. Fat substitute groups, combined, had lower body fat and higher body water as compared to controls. The O-FS group had lower serum glucose and insulin and higher fatty acid levels compared to the O-C group. There were no differences in serum cholesterol, HDL, or triglyceride levels due to fat substitute diet. These data suggest that the obese Zucker rat is unable to defend its body weight when dietary fat is replaced with sucrose polyester.
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PMID:Effects of a fat substitute, sucrose polyester, on food intake, body composition, and serum factors in lean and obese Zucker rats. 1635 28

Surveys have shown increases in dental caries in young persons in Kuwait. Intake of sugar and carbohydrates has increased, as has the incidence of obesity. The objective of this study was to identify dietary practices and the potential for dental disease in primary, intermediate, and secondary school students in a health region. A random sample of 600 students aged 8, 13, and 17 yrs in 12 schools (6 boys' schools and 6 girls' schools) received a questionnaire. Responses were analyzed by age group, gender, and dietary practices at home and in school. The dietary composition of meals tended to be similar at all ages and in both genders. A total of 97% of 8-yr-old, 96% of 13-yr-old, and 92% of 17-yr-old students reported snacking at school. Sugar intake from identified snacks alone was calculated as 193.8 g/day or the estimated equivalent of 746 calories, and daily fat intake was 70.17 g. A total of 88.6% of respondents (56.6% of all children) used fluoridated toothpaste; 44.4% of all children (22.6% of 8-yr-old, 14.1% of 13-yr-old, and 7.7% of 17-yr-old students) reported brushing their teeth three times per day. Use of school snacks increased with age, while use of a toothbrush decreased. Fundamental oral hygiene procedures such as brushing and use of fluoridated toothpaste appear to have been implemented. Health workers need to provide new and pertinent oral health messages, nutrition counseling, attention to diet, and reinforcement with parents, food preparers, health facilities, and intermediate and secondary schools.
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PMID:Dietary habits of the primary to secondary school population and implications for oral health. 1684 70

Sucrose-fed rats (1) had higher intra-abdominal fat mass and plasma non-esterified fatty acids and lower testosterone levels, (2) were hypertensive, and (3) had lower plasma NO metabolites than controls. The lack of testosterone by castration of sucrose-fed rats decreased high blood pressure and circulating non-esterified fatty acids and increased NO metabolites. The administration of testosterone to castrated sucrose-fed rats restored hypertension, fat accumulation, and high-circulating non-esterified fatty acids, and lowered NO metabolite levels whereas estradiol treatment did not significantly affect these variables in castrated animals. This study proposes that the low levels of testosterone found in sucrose-fed rats are sufficient to maintain central obesity and increased circulating non-esterified fatty acids, which contribute to the development of hypertension in sucrose-fed rats by modulating the biosynthesis of NO.
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PMID:Effect of sex hormones on non-esterified fatty acids, intra-abdominal fat accumulation, and hypertension induced by sucrose diet in male rats. 1713 34

We tested whether the dominant intestinal sugar transporter GLUT2 was inhibited by intestinal luminal compounds that are inefficiently absorbed and naturally present in foods. Because of their abundance in fruits and vegetables, flavonoids were selected as model compounds. Robust inhibition of glucose and fructose transport by GLUT2 expressed in Xenopus laevis oocytes was produced by the flavonols myricetin, fisetin, the widely consumed flavonoid quercetin, and its glucoside precursor isoquercitrin [corrected]. IC50s for quercetin, myricetin, and isoquercitirin [corrected]were approximately 200- to 1000-fold less than glucose or fructose concentrations, and noncompetitive inhibition was observed. The two other major intestinal sugar transporters, GLUT5 and SGLT1, were unaffected by flavonoids. Sugar transport by GLUT2 overexpressed in pituitary cells and naturally present in Caco-2E intestinal cells was similarly inhibited by quercetin. GLUT2 was detected on the apical side of Caco-2E cells, indicating that GLUT2 was in the correct orientation to be inhibited by luminal compounds. Quercetin itself was not transported by the three major intestinal glucose transporters. Because the flavonoid quercetin, a food component with an excellent pharmacology safety profile, might act as a potent luminal inhibitor of sugar absorption independent of its own transport, flavonols show promise as new pharmacologic agents in the obesity epidemic.
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PMID:Inhibition of the intestinal glucose transporter GLUT2 by flavonoids. 1717 39


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