Paradoxical effects of a high sucrose diet: high energy intake and reduced body weight gain

Appetite ◽  
2001 ◽  
Vol 37 (3) ◽  
pp. 253-254 ◽  
Author(s):  
S. Goodson ◽  
J.C.G. Halford ◽  
H.C. Jackson ◽  
J.E. Blundell
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Body Weight Gain ◽  
High Energy ◽  
Reduced Body ◽  
High Energy Intake ◽  
Paradoxical Effects ◽  
Sucrose Diet ◽  
High Sucrose Diet ◽  
High Sucrose

scholarly journals Polymannuronic acid ameliorated obesity and inflammation associated with a high-fat and high-sucrose diet by modulating the gut microbiome in a murine model

2017 ◽  
Vol 117 (9) ◽  
pp. 1332-1342 ◽  
Author(s):  
Fang Liu ◽  
Xiong Wang ◽  
Hongjie Shi ◽  
Yuming Wang ◽  
Changhu Xue ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Gut Microbiome ◽  
Body Weight Gain ◽  
High Fat ◽  
Microbial Composition ◽  
The Metabolic Syndrome ◽  
Sucrose Diet ◽  
High Sucrose Diet ◽  
High Sucrose

AbstractPolymannuronic acid (PM), one of numerous alginates isolated from brown seaweeds, is known to possess antioxidant activities. In this study, we examined its potential role in reducing body weight gain and attenuating inflammation induced by a high-fat and high-sucrose diet (HFD) as well as its effect on modulating the gut microbiome in mice. A 30-d PM treatment significantly reduced the diet-induced body weight gain and blood TAG levels (P<0·05) and improved glucose tolerance in male C57BL/6J mice. PM decreased lipopolysaccharides in blood and ameliorated local inflammation in the colon and the epididymal adipose tissue. Compared with low-fat and low-sucrose diet (LFD), HFD significantly reduced the mean number of species-level operational taxonomic units (OTU) per sample as well as species richness (P<0·05) but did not appear to affect other microbial diversity indices. Moreover, compared with LFD, HFD altered the abundance of approximately 23 % of the OTU detected (log10 linear discriminant analysis (LDA) score>2·0). PM also had a profound impact on the microbial composition in the gut microbiome and resulted in a distinct microbiome structure. For example, PM significantly increased the abundance of a probiotic bacterium, Lactobacillus reuteri (log10 LDA score>2·0). Together, our results suggest that PM may exert its immunoregulatory effects by enhancing proliferation of several species with probiotic activities while repressing the abundance of the microbial taxa that harbor potential pathogens. Our findings should facilitate mechanistic studies on PM as a potential bioactive compound to alleviate obesity and the metabolic syndrome.

Reduced insulin suppression of glucose appearance is related to susceptibility to dietary obesity in rats

1997 ◽  
Vol 272 (4) ◽  
pp. R1264-R1270 ◽  
Author(s):  
M. J. Pagliassotti ◽  
T. J. Horton ◽  
E. C. Gayles ◽  
T. A. Koppenhafer ◽  
T. D. Rosenzweig ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Weight Gain ◽  
Energy Intake ◽  
Body Weight Gain ◽  
Hepatic Insulin Resistance ◽  
Glucose Kinetics ◽  
Sucrose Diet ◽  
High Sucrose Diet ◽  
High Sucrose

To examine the relationship between insulin action and body weight regulation in male rats, the following studies were performed. In study 1, rats (n = 31) were fed a low-fat diet (LFD) for 4 wk, and then glucose kinetics were estimated under basal and hyperinsulinemic conditions using the glucose clamp. After clamps, these same rats were placed on a high-fat diet (HFD) for 5 wk. In study 2, rats (n = 30) were fed an LFD for 3 wk and then a high-sucrose diet for 1 wk to produce selective hepatic insulin resistance. Clamps were then performed, and after clamps, these same rats were placed on an HFD for 5 wk. In study 3, rats (n = 30) were fed an LFD for 1 wk and then a high-sucrose diet for 3 wk to produce widespread insulin resistance. Clamps were then performed, and after clamps, these same rats were placed on an HFD for 5 wk. The rate of glucose appearance (R(a)) during the hyperinsulinemic clamps was the only pre-HFD variable that correlated (r = 0.49, P < 0.01 in study 1; r = 0.51, P < 0.001 in study 2) with weight gain on the HFD. Clamp R(a) also correlated with energy intake on the HFD in study 1 (r = 0.64, P < 0.001) and study 2 (r = 0.59, P < 0.001). Clamp R(a) and energy intake on the HFD accounted for similar portions of the variance in body weight gain on the HFD. Weight gain and fat-pad mass were increased (P < 0.05) in study 2 compared with study 1. In study 3, pre-HFD glucose kinetics were not correlated with energy intake or weight gain on the HFD. Widespread insulin resistance did not significantly reduce the rate of weight gain on the HFD. Thus insulin action on R(a) can influence body weight gain on an HFD. The effects of R(a) on body weight gain appear to be mediated via effects on energy intake. Selective hepatic insulin resistance can increase body weight gain on an HFD, but widespread insulin resistance does not significantly reduce HFD-induced weight gain.

scholarly journals Diet-dependence of metabolic perturbations mediated by the endocrine disruptor tolylfluanid

2018 ◽  
Vol 7 (1) ◽  
pp. 159-168 ◽  
Author(s):  
Shane M Regnier ◽  
Andrew G Kirkley ◽  
Daniel Ruiz ◽  
Wakanene Kamau ◽  
Qian Wu ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Insulin Sensitivity ◽  
Glucose Homeostasis ◽  
Dietary Exposure ◽  
Visceral Adiposity ◽  
Obesity And Diabetes ◽  
Sucrose Diet ◽  
High Sucrose Diet ◽  
High Sucrose

Emerging evidence implicates environmental endocrine-disrupting chemicals (EDCs) in the pathogenesis of metabolic diseases such as obesity and diabetes; however, the interactions between EDCs and traditional risk factors in disease pathogenesis remain incompletely characterized. The present study interrogates the interaction of the EDC tolylfluanid (TF) and traditional dietary stressors in the promotion of metabolic dysfunction. Eight-week-old male C57BL/6 mice were fed a high-fat, high-sucrose diet (HFHSD) or a high-sucrose diet (HSD), with or without TF supplementation at 100 μg/g, for 12 weeks. Food intake, body weight and visceral adiposity were quantified. Glucose homeostasis was interrogated by intraperitoneal glucose and insulin tolerance tests at 9 and 10 weeks of exposure, respectively. After 12 weeks of dietary exposure, metabolic cage analyses were performed to interrogate nutrient handling and energy expenditure. In the background of an HFHSD, TF promoted glucose intolerance; however, weight gain and insulin sensitivity were unchanged, and visceral adiposity was reduced. In the background of an HSD, TF increased visceral adiposity; however, glucose tolerance and insulin sensitivity were unchanged, while weight gain was reduced. Thus, these analyses reveal that the metabolic perturbations induced by dietary exposure to TF, including the directionality of alterations in body weight gain, visceral adiposity and glucose homeostasis, are influenced by dietary macronutrient composition, suggesting that populations may exhibit distinct metabolic risks based on their unique dietary characteristics.

scholarly journals Synergistic Effects of DHA and Sucrose on Body Weight Gain in PUFA-Deficient Elovl2 -/- Mice

Nutrients ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 852
Author(s):  
Pauter ◽  
Fischer ◽  
Bengtsson ◽  
Asadi ◽  
Talamonti ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Body Weight Gain ◽  
Synergistic Effects ◽  
Plasma Lipoproteins ◽  
Sucrose Content ◽  
Omega 3 ◽  
High Sucrose

The omega-3 polyunsaturated fatty acid docosahexaenoic acid (DHA) is implicated in theregulation of both lipid and carbohydrate metabolism. Thus, we questioned whether dietary DHAand low or high content of sucrose impact on metabolism in mice deficient for elongation of verylong-chain fatty acids 2 (ELOVL2), an enzyme involved in the endogenous DHA synthesis. Wefound that Elovl2 -/- mice fed a high-sucrose DHA-enriched diet followed by the high sucrose, highfat challenge significantly increased body weight. This diet affected the triglyceride rich lipoproteinfraction of plasma lipoproteins and changed the expression of several genes involved in lipidmetabolism in a white adipose tissue. Our findings suggest that lipogenesis in mammals issynergistically influenced by DHA dietary and sucrose content.

scholarly journals Stress facilitates body weight gain in genetically predisposed rats on medium-fat diet

2003 ◽  
Vol 285 (4) ◽  
pp. R791-R799 ◽  
Author(s):  
Chantal Michel ◽  
Barry E. Levin ◽  
Ambrose A. Dunn-Meynell
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Dentate Gyrus ◽  
Energy Homeostasis ◽  
Body Weight Gain ◽  
High Energy ◽  
The Body ◽  
Central Nucleus ◽  
Sprague Dawley ◽  
Dorsomedial Nucleus

To assess the interaction between stress and energy homeostasis, we immobilized male Sprague-Dawley rats prone to diet-induced obesity (DIO) or diet resistance (DR) once for 20 min and then fed them either low-fat (4.5%) chow or a medium-fat (31%), high-energy (HE) diet for 9 days. Stressed, chow-fed DIO rats gained less, while stressed DIO rats on HE diet gained more body weight and had higher feed efficiency and plasma leptin levels than unstressed controls. Neither stress nor diet affected DR body weight gain. While stress-induced plasma corticosterone levels did not differ between phenotypes, DIO rats were initially more active in an open field and had higher hippocampal dentate gyrus and CA1 glucocorticoid receptor (GR) mRNA than DR rats, regardless of prior stress or diet. HE diet intake was associated with raised dentate gyrus and CA1 GR and amygdalar central nucleus (CeA) corticotropin-releasing hormone (CRH) mRNA expression, while stress was associated with reduced hypothalamic dorsomedial nucleus Ob-R mRNA and CeA CRH specifically in DIO rats fed HE diet. Thus a single stress triggers a complex interaction among weight gain phenotype, diet, and stress responsivity, which determines the body weight and adiposity of a given individual.

scholarly journals Effect of Heat Stress on Body Weight Gain, Heterophile-Lymphocite Ratio and Body Temperature in Broiler

2016 ◽  
Vol 3 (1) ◽  
Author(s):  
Sugito S ◽  
Mira Delima
Keyword(s):  
Body Weight ◽  
Heat Stress ◽  
Weight Gain ◽  
Body Temperature ◽  
Broiler Chicken ◽  
Body Weight Gain ◽  
Conversion Ratio ◽  
Feed Conversion Ratio ◽  
Feed Conversion ◽  
Reduced Body

Increasing in ambient temperature inside the cage could lead to heat stress in broilers. This research was conducted to find out effects of heat stress on body weight gain, heterophile-lymphocite ratio and body temperature in chicken broiler. Twenty broilers aged 20 days (strain Cobb) were randomly divided into 2 groups. The first group was treated with no heat stress, the second one was caged in 33±1 0C temperature for 4 hours per day for 14 days. The results indicated that heat stress reduced body weight gain, increased body temperature, and changed behavior, but no effect on feed conversion ratio (FCR) and heterophile-lymphocyte ratio. It suggested that the heat stress caused detrimental effects on broiler chicken.

scholarly journals Cigarette smoking blocks the benefit from reduced weight gain for insulin action by shifting lipids deposition to muscle

2020 ◽  
Vol 134 (13) ◽  
pp. 1659-1673
Author(s):  
Anwar Khan ◽  
Sherouk Fouda ◽  
Ali Mahzari ◽  
Stanley M.H. Chan ◽  
Xiu Zhou ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Cigarette Smoking ◽  
Mrna Expression ◽  
Glucose Intolerance ◽  
Insulin Action ◽  
Insulin Signalling ◽  
Body Weight Gain ◽  
Hormone Sensitive Lipase ◽  
Reduced Body

Abstract Cigarette smoking (CS) is known to reduce body weight and this often masks its real effect on insulin action. The present study tested the hypothesis that CS can divert lipid deposition to muscles to offset the supposed benefit of reduced body weight gain on insulin signalling in this major site for glucose tolerance (or insulin action). The study was conducted in mice exposed to chronic CS followed by either a chow (CH) diet or a high-fat (HF) diet. CS increased triglyceride (TG) levels in both plasma and muscle despite a reduced body weight gain and adiposity. CS led to glucose intolerance in CH-fed mice and they retained the glucose intolerance that was induced by the HF diet. In adipose tissue, CS increased macrophage infiltration and the mRNA expression of TNFα but suppressed the protein expression of adipose triglyceride lipase and PPARγ. While CS increased hormone-sensitive lipase and suppressed the mRNA expression of leptin, these effects were blunted in HF-fed mice. These results imply that CS impairs insulin signalling in skeletal muscle via accumulated intramuscular lipids from lipolysis and lipodystrophy of adipose tissues. This may explain why smokers may not benefit from insulin sensitising effects of reduced body weight gain.

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