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 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.

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 Influence of Saskatoon Berry and Cyanidin-3-Glucoside on Gut Microbiota and Relationship with Metabolism and Inflammation in High Fat-High Sucrose Diet-Induced Insulin Resistant Mice

2020 ◽  
Author(s):  
Fei Huang ◽  
Ruozhi Zhao ◽  
Mi Xia ◽  
Garry Shen
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Gut Microbiota ◽  
Inflammatory Mediators ◽  
Inflammatory Markers ◽  
High Fat ◽  
Insulin Resistant ◽  
Sucrose Diet ◽  
High Sucrose Diet ◽  
High Sucrose

Abstract Background Type 2 Diabetes (T2D) has become one of most common and harmful chronic diseases worldwide. T2D is characterized as insulin resistant and is often associated with unhealthy dietary habits. The present study assessed the effects of freeze-dried Saskatoon berry powder (SBp) and cyanidin-3-glucoside (C3G, an anthocyanin enriched in SBp) on metabolism, inflammatory markers and gut microbiota in high fat-high sucrose diet (HFHS) diet induced insulin resistant mice. Results Male C57 BL/6J mice received control, HFHS, HFHS + SBp (8.0 g/kg body weight/day) or HFHS + C3G (7.2 mg/kg/day, equal amount of C3G in 8.0 g/kg/day SBp) diet for 11 weeks. HFHS diet significantly increased the levels of glucose, cholesterol, triglycerides, insulin resistance and inflammatory mediators in plasma. The results of 16S rRNA gene sequencing demonstrated that HFHS diet increased the ratio of Bacteroidetes/Firmicutes (B/F) phylum bacteria and an elevated abundance of Muriculaceae family bacteria in the feces of mice. SBp or C3G supplementation attenuated HFHS diet-induced disorders in metabolism and inflammatory markers, and increased B/F ratio and Muriculaceae abundance in mouse gut compared to HFHS diet alone. The abundance of Muriculaceae in the gut microbiota negatively correlated with body weight, glucose, lipids, insulin resistance and inflammatory mediators in mice. The results of functional predication analysis suggest that HFHS diet upregulated the genes of gut bacteria involved in inflammation-related cellular processes, and inhibited bacteria involved in metabolism. SBp and C3G partially neutralized the alterations induced by HFHS diet in gut microbiota implicated in metabolism or inflammation. Conclusion The findings of the present study suggest that SBp is a potential prebiotic food mitigating Western diet-induced disorders in metabolism, inflammation and gut dysbiosis, and C3G possibly contributes to the beneficial effects of SBp.

Increased net hepatic glucose output from gluconeogenic precursors after high-sucrose diet feeding in male rats

1997 ◽  
Vol 272 (2) ◽  
pp. R526-R531 ◽  
Author(s):  
M. J. Pagliassotti ◽  
P. A. Prach
Keyword(s):  
Insulin Resistance ◽  
Glucose Production ◽  
Male Rats ◽  
Hepatic Insulin Resistance ◽  
Hepatic Glucose Output ◽  
Hepatic Glucose ◽  
Sucrose Diet ◽  
High Sucrose Diet ◽  
Glucose Output ◽  
High Sucrose

A high-sucrose diet reduces the ability of insulin to suppress hepatic glucose production (hepatic insulin resistance) in rats. The purpose of the present study was to investigate the contribution of hepatic gluconeogenesis to sucrose-induced hepatic insulin resistance. Single-pass liver perfusions were performed on 24-h food-deprived male Wistar rats after 8 wk on either a high-corn starch (ST; 68% of energy) or high-sucrose (SU; 68% of energy) diet. Hepatic glucose output (HGO, micromol of glucose x min(-1) x g(-1)) in the presence of lactate, alanine, or dihydroxyacetone (DHA) was used as an estimate of gluconeogenic capacity, because liver glycogen levels after the 24-h fast were negligible (<1.2 mg/g). HGO was significantly (P < 0.05) greater in SU vs. ST at all concentrations of lactate, alanine, and DHA. Maximal rates of HGO were 1.9 +/- 0.4 and 2.8 +/- 0.3 at 10 mM lactate, 0.6 +/- 0.2 and 1.4 +/- 0.3 at 10 mM alanine, and 1.7 +/- 0.3 and 2.6 +/- 0.2 at 20 mM DHA in ST and SU, respectively. When HGO was matched between SU and ST with the use of different precursor concentrations, there was a significant (P < 0.05) reduction in the ability of insulin (175 microU/ml) to suppress HGO in SU vs. ST. These data suggest that sucrose feeding increases gluconeogenesis from lactate, alanine, and DHA and that this route of glucose production is resistant to insulin suppression.

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 Sexual dimorphism in insulin resistance in a metabolic syndrome rat model

2020 ◽  
Vol 9 (9) ◽  
pp. 890-902
Author(s):  
Myrian Velasco ◽  
Rosa Isela Ortiz-Huidobro ◽  
Carlos Larqué ◽  
Yuriko Itzel Sánchez-Zamora ◽  
José Romo-Yáñez ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Rat Model ◽  
Molecular Mechanisms ◽  
Body Weight Gain ◽  
Liver Steatosis ◽  
Phosphorylated Akt ◽  
Sucrose Diet ◽  
High Sucrose Diet ◽  
High Sucrose

Objective: We assessed the sex-specific differences in the molecular mechanisms of insulin resistance in muscle and adipose tissue, in a MS rat model induced by a high sucrose diet. Methods: Male, female, and ovariectomized female Wistar rats were randomly distributed in control and high-sucrose diet (HSD) groups, supplemented for 24 weeks with 20% sucrose in the drinking water. At the end, we assessed parameters related to MS, analyzing the effects of the HSD on critical nodes of the insulin signaling pathway in muscle and adipose tissue. Results: At the end of the treatment, HSD groups of both sexes developed obesity, with a 15, 33 and 23% of body weight gain in male, female, and OVX groups respectively, compared with controls; mainly related to hypertrophy of peripancreatic and gonadal adipose tissue. They also developed hypertriglyceridemia, and liver steatosis, with the last being worse in the HSD females. Compared to the control groups, HSD rats had higher IL1B and TNFA levels and insulin resistance. HSD females were more intolerant to glucose than HSD males. Our observations suggest that insulin resistance mechanisms include an increase in phosphorylated AKT(S473) form in HSD male and female groups and a decrease in phosphorylated P70S6K1(T389) in the HSD male groups from peripancreatic adipose tissue. While in gonadal adipose tissue the phosphorylated form of AKT decreased in HSD females, but not in HSD males. Finally, HSD groups showed a reduction in p-AKT levels in gastrocnemius muscle. Conclusion: A high-sucrose diet induces MS and insulin resistance with sex-associated differences and in a tissue-specific manner.

The prophylactic potential of Zingiber officinale flowers and leaves extract to mitigate hyperglycemia in Sprague Dawley rats

2021 ◽  
Vol ahead-of-print (ahead-of-print) ◽  
Author(s):  
Saira Tanweer ◽  
Tariq Mehmood ◽  
Saadia Zainab ◽  
Zulfiqar Ahmad ◽  
Muhammad Ammar Khan ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Weight Gain ◽  
Body Weight Gain ◽  
Zingiber Officinale ◽  
Sprague Dawley ◽  
Content Type ◽  
Sprague Dawley Rats ◽  
Hematological Analysis ◽  
Therapeutic Tools

Purpose Innovative health-promoting approaches of the era have verified phytoceutics as one of the prime therapeutic tools to alleviate numerous health-related ailments. The purpose of this paper is to probe the nutraceutic potential of ginger flowers and leaves against hyperglycemia. Design/methodology/approach The aqueous extracts of ginger flowers and leaves were observed on Sprague Dawley rats for 8 weeks. Two parallel studies were carried out based on dietary regimes: control and hyperglycemic diets. At the end of the experimental modus, the overnight fed rats were killed to determine the concentration of glucose and insulin in serum. The insulin resistance and insulin secretions were also calculated by formulae by considering fasting glucose and fasting insulin concentrations. Furthermore, the feed and drink intakes, body weight gain and hematological analysis were also carried out. Findings In streptozotocin-induced hyperglycemic rats, the ginger flowers extract depicted 5.62% reduction; however, ginger leaves extract reduced the glucose concentration up to 7.11% (p = 0.001). Similarly, ginger flowers extract uplifted the insulin concentration up to 3.07%, while, by ginger leaves extract, the insulin value increased to 4.11% (p = 0.002). For the insulin resistance, the ginger flower showed 5.32% decrease; however, the insulin resistance was reduced to 6.48% by ginger leaves (p = 0.014). Moreover, the insulin secretion increased to 18.9% by flower extract and 21.8% by ginger leave extract (p = 0.001). The feed intake and body weight gain increased momentously by the addition of ginger flowers and leaves; however, the drink intake and hematological analysis remained non-significant by the addition of ginger parts. Originality/value Conclusively, it was revealed that leaves have more hypoglycemic potential as compared to flowers.

scholarly journals Eicosapentaenoic acid actions on adiposity and insulin resistance in control and high-fat-fed rats: role of apoptosis, adiponectin and tumour necrosis factor-α

2007 ◽  
Vol 97 (2) ◽  
pp. 389-398 ◽  
Author(s):  
Patricia Pérez-Matute ◽  
Nerea Pérez-Echarri ◽  
J. Alfredo Martínez ◽  
Amelia Marti ◽  
María J. Moreno-Aliaga
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Body Weight Gain ◽  
Control Diet ◽  
Cafeteria Diet ◽  
High Fat ◽  
Beneficial Effects

n-3 PUFA have shown potential anti-obesity and insulin-sensitising properties. However, the mechanisms involved are not clearly established. The aim of the present study was to assess the effects of EPA administration, one of the n-3 PUFA, on body-weight gain and adiposity in rats fed on a standard or a high-fat (cafeteria) diet. The actions on white adipose tissue lipolysis, apoptosis and on several genes related to obesity and insulin resistance were also studied. Control and cafeteria-induced overweight male Wistar rats were assigned into two subgroups, one of them daily received EPA ethyl ester (1 g/kg) for 5 weeks by oral administration. The high-fat diet induced a very significant increase in both body weight and fat mass. Rats fed with the cafeteria diet and orally treated with EPA showed a marginally lower body-weight gain (P = 0·09), a decrease in food intake (P < 0·01) and an increase in leptin production (P < 0·05). EPA administration reduced retroperitoneal adipose tissue weight (P < 0·05) which could be secondary to the inhibition of the adipogenic transcription factor PPARγ gene expression (P < 0·001), and also to the increase in apoptosis (P < 0·05) found in rats fed with a control diet. TNFα gene expression was significantly increased (P < 0·05) by the cafeteria diet, while EPA treatment was able to prevent (P < 0·01) the rise in this inflammatory cytokine. Adiposity-corrected adiponectin plasma levels were increased by EPA. These actions on both TNFα and adiponectin could explain the beneficial effects of EPA on insulin resistance induced by the cafeteria diet.

scholarly journals Individual housing of male C57BL/6J mice after weaning impairs growth and predisposes for obesity

2019 ◽  
Author(s):  
Lidewij Schipper ◽  
Steffen van Heijningen ◽  
Giorgio Karapetsas ◽  
Eline M. van der Beek ◽  
Gertjan van Dijk
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Energy Intake ◽  
White Adipose Tissue ◽  
Body Weight Gain ◽  
Tissue Mass ◽  
Individual Housing ◽  
Adipose Tissue Mass ◽  
Obesogenic Diet

AbstractIndividual housing from weaning onwards resulted in reduced growth rate during adolescence in male C57Bl/6J mice that were housed individually, while energy intake and energy expenditure were increased compared to socially housed counterparts. At 6 weeks of age, these mice had reduced lean body mass, but significantly higher white adipose tissue mass compared to socially housed mice. Body weight gain of individually housed animals exceeded that of socially housed mice during adulthood, with elevations in both energy intake and expenditure. At 18 weeks of age, individually housed mice showed higher adiposity and higher mRNA expression of UCP-1 in inguinal white adipose tissue. Exposure to an obesogenic diet starting at 6 weeks of age further amplified body weight gain and adipose tissue deposition. This study shows that post-weaning individual housing of male mice results in impaired adolescent growth and higher susceptibility to obesity in adulthood. Mice are widely used to study obesity and cardiometabolic comorbidities. For (metabolic) research models using mice, (social) housing practices should be carefully considered and regarded as a potential confounder due to their modulating effect on metabolic health outcomes.

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