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

Adult male rats were fed, in addition to chow and water, solutions (32%) of either sucrose, Polycose (a bland-tasting polysaccharide), or Polycose sweetened with 0.2% saccharin. The solutions were available for two 30-day periods when the rats were 90-120, and 180-210 days of age. A control group received only chow and water during these periods. During the second 30-day test the Polycose and Saccharin- Polycose groups were hyperphagic and gained as much excess weight as did the Sucrose group. The sucrose-fed rats, however, did not overeat relative to the control animals. Adding saccharin to the Polycose failed to increase total caloric intake or weight gain, but did increase Polycose intake and percent carbohydrate intake. The intakes of both Polycose solutions were greater than that of the sucrose solution, although in brief two-bottle preference tests the sucrose solution was preferred over the Polycose and saccharin- Polycose solutions. A similar pattern of results was obtained during the first test period, but the group differences were less pronounced. The findings demonstrate that carbohydrate-induced obesity is not unique to sweet-tasting sugars, but can also be produced by bland-tasting polysaccharides. Sweet taste does increase polysaccharide preference and intake, however.
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PMID:Sucrose and polysaccharide induced obesity in the rat. 653 78

During cold-induced nonshivering thermogenesis, interscapular brown adipose tissue (BAT) lipoprotein lipase (LPL) activity and lipogenesis are elevated. Because of the many similarities between cold- and diet-induced thermogenesis, we examined the effect of ad libitum access to a 32% sucrose solution on caloric intake, adiposity, and BAT enzyme activities in male rats. Daily caloric intakes of sucrose-fed animals were elevated by 20%-25%, and 8 wk of sucrose feeding doubled carcass fat content. This sucrose-feeding induced obesity was associated with increases in circulating triglyceride and insulin levels as well as increased retroperitoneal white adipose tissue LPL activity. However, the increased carcass lipid content accounted for less than half of the excess calories ingested by the sucrose-fed rats. Sucrose feeding stimulated in vivo lipogenesis in BAT and elevated BAT fatty acid synthetase and acetyl-CoA carboxylase activities but not LPL activity. These findings suggest that overeating enhances endogenous lipogenesis but not uptake of circulating triglyceride in BAT. Thus, both cold- and diet-induced thermogenesis increase BAT lipogenesis, while only cold-induced thermogenesis is associated with elevated LPL activity in BAT.
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PMID:Effect of sucrose overfeeding on brown adipose tissue lipogenesis and lipoprotein lipase activity in rats. 682 91

When male golden hamsters were switched from a diet of Purina rodent chow to a calorically-dense high-fat diet or were given ad lib access to a 32% sucrose solution in addition to chow, they adjusted their food intakes rapidly (within 24 hr) and did not overeat. Nevertheless, the fat-fed hamsters tripled their rate of weight gain and nearly doubled their carcass fat content after one month on the diet. Resting oxygen consumption (animals awake but quite) was significantly lower in fat-fed animals than in chow-fed controls. Sucrose feeding had no effect on food intake, body weight gain, carcass composition or oxygen consumption. Thus, whereas rats exhibit dietary obesity in spite of increases in energy expenditure (diet-induced thermogenesis), fat-fed hamsters seem to become obese because of decreases in energy expenditure. However, although actual energy expenditure is reduced, fat-fed hamsters exhibit an enhanced thermogenic capacity. Interscapular brown adipose tissue mass, protein content, and DNA content as well as norepinephrine-stimulated oxygen consumption were all significantly elevated in fat-fed hamsters. The significance of these concurrent diet-induced decreases in energy expenditure and increases in thermogenic capacity is not clear, but they could be of some value in preparing the hamster for winter.
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PMID:Obesity without overeating in golden hamsters. 689 Oct 78

Sucrose consumption is a controversial issue. Part of the difficulty arises because of inadequate knowledge about the actual consumption of populations, as well as individuals within a population. Data on the sucrose content of foods are lacking. This review presents information published in the 1970s on these topics as well as current research and thinking about possible relationships of sucrose consumption to dental caries, cardiovascular disease, diabetes, obesity, and other disease conditions. Current attitudes toward recommendations concerning sugar consumption in the U.S. Dietary Goals are examined, as are data on the use of sugar as a fortification vehicle.
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PMID:The nutrition significance of sucrose consumption, 1970-1980. 700 64

We evaluated the course of diabetes and nephropathy in the SHR/N-cp (corpulent) rat characterized by genetic obesity, non-insulin-dependent diabetes (NIDDM), and hypertension, and examined whether the nephropathy in this model is influenced by the type of carbohydrate intake. Two groups of obese and lean SHR/N-cp rats were fed diets containing 54% carbohydrate, as either sucrose or starch for 3 months (group I) and 9 months (group II). After 3 months on either diet, group I obese rats had higher 2-h response serum glucose levels and urinary glucose excretion than lean rats. Sucrose feeding was associated with greater proteinuria and a higher percentage of abnormal glomeruli in obese rats. Morphometric evaluation of glomeruli (by computerized image analysis) showed greater mean renal corpuscular volume and mesangial fraction in obese than in lean rats fed similar diets. Mean renal corpuscular volume and mesangial fraction were also greater in sucrose-fed obese rats than in starch-fed obese rats. After 9 months, group II obese rats had substantial reductions in serum and urine glucose levels but they were still hyperinsulinaemic and showed more proteinuria than lean rats and a higher percentage of sclerotic glomeruli compared with group I obese rats. At this time, mean mesangial fraction but not renal corpuscular volume was still higher in obese than in lean rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diabetic glomerulopathy in the SHR/N-corpulent rat: role of dietary carbohydrate in a model of NIDDM. 774 27

To determine the effects of sucrose-enriched feeds on somatic growth, blood pressure development, and insulin-stimulated glucose metabolism, Sprague-Dawley rat pups (n = 94) were randomly assigned at weaning (3 wk) to a control diet (15% sucrose, by calories, n = 48) or an isocaloric diet in which starch is replaced by sucrose (66% sucrose, by calories, n = 46). Weight and blood pressure were followed until 13 wk. Chronic catheters were placed in a subset of male animals (n = 13), fasting glucose production was measured, and euglycemic hyperinsulinemic clamps were performed while the rats were in the conscious, nonstressed state. There was no difference in weight gain between control and sucrose rats in each sex group. Blood pressure in sucrose rats was significantly higher than in control rats after 4 wk of diet (7 wk of age, p < 0.001) in both sex groups and persisted for the duration of sucrose-enriched feeds. Insulin resistance was confirmed in sucrose rats with the euglycemic hyperinsulinemic clamp technique. In juvenile rats that have no genetic predisposition to hypertension, excess dietary sucrose induced high blood pressure without obesity. Sucrose feeding also induced insulin resistance. The sucrose-fed Sprague-Dawley weanling rat provides a model
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PMID:The effect of excess dietary sucrose on growth, blood pressure, and metabolism in developing Sprague-Dawley rats. 793 45

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

Differing risk factors between men and women for a number of vascular and metabolic diseases have been linked to regional obesity. The differences in the distribution of adipose tissues between men (abdominal or upper-body obesity) and women (gluteal/femoral or lower body obesity) suggest a role for sex steroids in the regional distribution of fat. Previous work from this laboratory has shown the presence of oestrogen receptor (ER) in gluteal, perirenal and omental adipose tissues of ewes with similar physical characteristics to the ER in uterine tissue. The concentration profile for adipose ER was gluteal > perirenal > omental. In this report, we determined the physiological significance of adipose ERs by showing an up-regulation of the progesterone receptor (PR) in adipose tissues after oestrogen treatment in a fashion similar to that seen in a major responsive tissue such as uterus. Using PR antibodies (PR-6 and C-262), Western blot analysis of PR from oestrogen-treated sheep indicated that PR was induced in uterus >>> gluteal adipose > perirenal adipose consistent with the concentration of ER contained in these tissues. PR could not be detected by Western blotting in omental adipose tissue from oestrogen-treated animals or in gluteal, perirenal and omental adipose tissues from untreated animals. Sucrose gradient profiles of progestin (R-5020) binding from uterus and gluteal adipose tissues of oestrogen-treated ewes showed specific binding in both the 5S and 9S regions of the gradient, while perirenal and omental adipose tissue had only the 5S peak. The amount of specific binding was increased with oestrogen treatment in all the tissues. When gluteal adipose tissue cytosol was preincubated with PR antibody (C-262) to prevent binding of ligand and subjected to sucrose gradient analysis, both the 5S and 9S regions were diminished, suggesting that both peaks contained PR. Dilution of uterine cytosol resulted in an increase in the ratio of the 5S to the 9S peak, indicating that the 9S PR complex dissociates at low concentrations; this may be the reason why only the 5S peak was observed in perirenal and omental adipose tissues. These data offer further support for a direct role of sex steroids in regional adipose accretion and metabolism.
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PMID:Regional differences and up-regulation of progesterone receptors in adipose tissues from oestrogen-treated sheep. 856 67

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

Albright hereditary osteodystrophy (AHO), a disorder characterized by skeletal abnormalities and obesity, is associated with heterozygous inactivating mutations in the gene for Gsalpha. A novel Gsalpha mutation encoding the substitution of tryptophan for a nonconserved arginine within the switch 3 region (Gsalpha R258W) was identified in an AHO patient. Although reverse transcription-polymerase chain reaction studies demonstrated that mRNA expression from wild type and mutant alleles was similar, Gsalpha expression in erythrocyte membranes from the affected patient was reduced by 50%. A Gsalpha R258W cDNA, as well as one with arginine replaced by alanine (Gsalpha R258A), was generated, and the biochemical properties of in vitro transcription/translation products were examined. When reconstituted with cyc- membranes, both mutant proteins were able to stimulate adenylyl cyclase normally in the presence of guanosine- 5'-O-(3-thiotriphosphate) (GTPgammaS) but had decreased ability in the presence of isoproterenol or AlF4- (a mixture of 10 microM AlCl3 and 10 mM NaF). The ability of each mutant to bind and be activated by GTPgammaS or AlF4- was assessed by trypsin protection assays. Both mutants were protected normally by GTPgammaS but showed reduced protection in the presence of AlF4-. The addition of excess GDP (2 mM) was able to rescue the ability of AlF4- to protect the mutants, suggesting that they might have reduced affinity for GDP. A Gsalpha R258A mutant purified from Escherichia coli had decreased affinity for GDP and an apparent rate of GDP release that was 10-fold greater than that of wild type Gsalpha. Sucrose density gradient analysis demonstrated that both Gsalpha R258W and Gsalpha R258A were thermolabile at higher temperatures and that denaturation of both mutants was prevented by the presence of 0.1 mM GTPgammaS or 2 mM GDP. The crystal structure of Gsalpha demonstrates that Arg258 interacts with a conserved residue in the helical domain (Gln170). Arg258 substitutions would be predicted to open the cleft between the GTPase and helical domains, allowing for increased GDP release in the inactive state, resulting in enhanced thermolability and reduced AlF4--induced adenylyl cyclase stimulation and trypsin protection, since activation by AlF4- requires bound GDP.
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PMID:A novel mutation in the switch 3 region of Gsalpha in a patient with Albright hereditary osteodystrophy impairs GDP binding and receptor activation. 972 13


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