Inulin fiber dose-dependently modulates energy balance, glucose tolerance, gut microbiota, hormones and diet preference in high-fat-fed male rats

2018 ◽  
Vol 59 ◽  
pp. 142-152 ◽  
Author(s):  
Arashdeep Singh ◽  
Rizaldy C. Zapata ◽  
Adel Pezeshki ◽  
Roger D. Reidelberger ◽  
Prasanth K. Chelikani
Keyword(s):  
Energy Balance ◽  
Glucose Tolerance ◽  
Gut Microbiota ◽  
Male Rats ◽  
High Fat ◽  
Diet Preference

scholarly journals Beneficial Effects of Non-Encapsulated or Encapsulated Probiotic Supplementation on Microbiota Composition, Intestinal Barrier Functions, Inflammatory Profiles, and Glucose Tolerance in High Fat Fed Rats

Nutrients ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 1975 ◽  
Author(s):  
Sunhye Lee ◽  
Rebecca Kirkland ◽  
Zachary I. Grunewald ◽  
Qingshen Sun ◽  
Louise Wicker ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Gut Microbiota ◽  
Male Rats ◽  
Microbiota Composition ◽  
High Fat ◽  
Probiotic Supplementation ◽  
Barrier Functions ◽  
Positive Effects ◽  
Probiotic Treatment ◽  
Gut Microbiota Composition

Development of obesity-associated comorbidities is related to chronic inflammation, which has been linked to gut microbiota dysbiosis. Thus, modulating gut microbiota composition could have positive effects for metabolic disorders, supporting the use of probiotics as potential therapeutics in vivo, which may be enhanced by a microencapsulation technique. Here we investigated the effects of non-encapsulated or pectin-encapsulated probiotic supplementation (Lactobacillus paracasei subsp. paracasei L. casei W8®; L. casei W8) on gut microbiota composition and metabolic profile in high-fat (HF) diet-fed rats. Four male Wistar rat groups (n = 8/group) were fed 10% low-fat, 45% HF, or HF with non-encapsulated or encapsulated L. casei W8 (4 × 107 CFU/g diet) diet for seven weeks. Microbiota composition, intestinal integrity, inflammatory profiles, and glucose tolerance were assessed. Non-encapsulated and pectin-encapsulated probiotic supplementation positively modulated gut microbiota composition in HF-fed male rats. These changes were associated with improvements in gut barrier functions and local and systemic inflammation by non-encapsulated probiotics and improvement in glucose tolerance by encapsulated probiotic treatment. Thus, these findings suggest the potential of using oral non-encapsulated or encapsulated probiotic supplementation to ameliorate obesity-associated metabolic abnormalities.

Abstract 58: Angiotensin-(1-7) Mas Receptors In The Arcuate Nucleus Of The Hypothalamus Protect Against High Fat Diet-induced Insulin Resistance In Female Mice

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Darren Mehay ◽  
Sarah Bingaman ◽  
Yuval Silberman ◽  
Amy Arnold
Keyword(s):  
Body Composition ◽  
Insulin Sensitivity ◽  
Energy Balance ◽  
Glucose Tolerance ◽  
High Fat Diet ◽  
Metabolic Regulation ◽  
Arcuate Nucleus ◽  
Control Diet ◽  
High Fat ◽  
Metabolic Outcomes

Angiotensin (Ang)-(1-7) is a protective hormone of the renin-angiotensin system that improves insulin sensitivity, glucose tolerance, and energy balance in obese rodents. Our recent findings suggest that Ang-(1-7) activates mas receptors (MasR) in the arcuate nucleus of the hypothalamus (ARC), a brain region critical to control of energy balance and glucose homeostasis, to induce these positive metabolic effects. The distribution of MasR in the ARC and their role in metabolic regulation, however, is unknown. We hypothesized: (1) MasR are expressed in the ARC; and (2) deletion of ARC MasR leads to worsened metabolic outcomes following high fat diet (HFD). To test this, male and female C57Bl/6J mice were fed a 60% HFD or matched control diet ad libitum for 12 weeks. RNAscope in situ hybridization was performed on coronal ARC sections in rostral-middle-caudal regions to determine percentage of MasR positive neurons (n=5/group). In a second experiment, we assessed body composition and insulin and glucose tolerance in transgenic mice with deletion of MasR in ARC neurons (MasR-flox with AAV5-hsyn-GFP-Cre). RNAscope revealed a wide distribution on MasR-positive cells throughout the rostral to caudal extent of the ARC. The average percentage of MasR positive neurons was increased in females versus males, with HFD tending to increase MasR expression in both sexes (control diet male: 11±2; control diet female: 17±3; HFD male: 15±5; HFD female: 24±2; p sex : 0.030; p diet : 0.066; p int : 0.615; two-way ANOVA). Deletion of MasR in ARC neurons worsened insulin sensitivity in HFD but not control diet females (area under the curve for change in glucose from baseline: -1989±1359 HFD control virus vs. 2530±1762 HFD Cre virus; p=0.016), while fasting glucose, glucose tolerance, and body composition did not change. There was no effect of ARC MasR deletion on metabolic outcomes in control diet or HFD male mice. These findings suggest females have more MasR positive neurons in the ARC compared to males, which may be a sex-specific protective mechanism for glucose homeostasis. While further studies are needed to explore the role of ARC MasR in metabolic regulation, these findings support targeting Ang-(1-7) as an innovative strategy in obesity.

scholarly journals Comparison of high-fat and high-carbohydrate diets for obtaining an experimental model of metabolic syndrome

2021 ◽  
Vol 15 (1) ◽  
pp. 3-14
Author(s):  
T. S. Petryn ◽  
◽  
M. R. Nagalievska ◽  
N. O. Sybirna ◽  
◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Glucose Tolerance ◽  
Pathological Condition ◽  
Male Rats ◽  
Laboratory Animals ◽  
Atherogenic Dyslipidemia ◽  
Chow Diet ◽  
High Fat ◽  
High Carbohydrate

Introduction. Metabolic syndrome is a cluster of metabolic abnormalities that includes hypertension, central obesity, insulin resistance and atherogenic dyslipidemia. Given the wide geographical distribution and growing number of people suffering from this disease, there is an urgent need in developing animal models that would accurately reproduce the development of all symptoms of human metabolic syndrome (insulin resistance, dyslipidemia, obesity and hypertension). The most cost-effective method related to the real causes of metabolic syndrome is the use of different types of diets. Materials and Methods. The study was performed on white outbred male rats about 6 months old and weighing 300–400 g. The metabolic syndrome was induced by high-fat and high-carbohydrate diets. The lipid-enriched diet involved the consumption of regular chow diet for laboratory animals with additional fat content (40 % by weight of chow). The source of additional lipids was olive oil, which is rich in monounsaturated fatty acids (MUFAs). Animals on the diet enriched in carbohydrates together with regular chow diet for laboratory animals consumed 10 % fructose solution instead of drinking water. Glucose tolerance tests were conducted and areas under the glycemic curves were calculated. We determined the content of glycated hemoglobin and glucose concent­ration, the concentration of low-density lipoproteins (LDL), high-density lipoproteins (HDL), triglycerides and cholesterol in the blood plasma of rats. Results. The development of metabolic syndrome induced by an excessive consumption of carbohydrates and lipids for 42 days was accompanied by impaired glucose tolerance, increased glycosylated hemoglobin, triglycerides and cholesterol concentrations, as well as a decreased HDL content. An increase in the concentrations of LDL and activity of paraoxonase were found due to the induction of the pathological condition by an excessive fat intake, while a high carbohydrate diet caused a decrease in paraoxonase activity. Conclusions. The use of fructose for 42 days causes the most pronounced manifestations of the studied pathology. The use of this model will allow determining the biochemical and molecular changes that accompany the development of this pathological condition. It will also facilitate the development and evaluation of the effectiveness of new therapeutic approaches to the treatment of metabolic syndrome.

Prevention of diet-induced obesity and impaired glucose tolerance in rats following administration of leptin to their mothers

2007 ◽  
Vol 292 (5) ◽  
pp. R1810-R1818 ◽  
Author(s):  
Claire J. Stocker ◽  
Ed Wargent ◽  
Jacqueline O'Dowd ◽  
Claire Cornick ◽  
John R. Speakman ◽  
...  
Keyword(s):  
Weight Gain ◽  
Energy Balance ◽  
Glucose Tolerance ◽  
Female Offspring ◽  
Male Offspring ◽  
Male Rats ◽  
Fat Pad ◽  
Plasma Insulin Concentration ◽  
Obesogenic Diet ◽  
Tolerance Curve

Absence of leptin is known to disrupt the development of energy balance regulatory mechanisms. We investigated whether administration of leptin to normally nourished rats affects energy balance in their offspring. Leptin (2 mg·kg−1·day−1) was administered from day 14 of pregnancy and throughout lactation. Male and female offspring were fed either on chow or on high-fat diets that elicited similar levels of obesity in the sexes from 6 wk to 15 mo of age. Treatment of the dams with leptin prevented diet-induced increases in the rate of weight gain, retroperitoneal fat pad weight, area under the intraperitoneal glucose tolerance curve, and fasting plasma insulin concentration in female offspring. In the male offspring, the diet-induced increase in weight gain was prevented and increased fat pad weight was reduced. Energy intake per rat was higher in response to the obesogenic diet in male offspring of saline-treated but not leptin-treated dams. A similar trend was seen in 3-mo-old female offspring. Energy expenditure at 3 mo of age was higher for a given body weight in female offspring of leptin-treated compared with saline-treated dams when these animals were fed on the obesogenic diet. A similar trend was seen for male rats fed on the obesogenic diet. Thus leptin levels during pregnancy and lactation can affect the development of energy balance regulatory systems in their offspring.

scholarly journals Effect of stevia on the gut microbiota and glucose tolerance in a murine model of diet-induced obesity

2020 ◽  
Vol 96 (6) ◽  
Author(s):  
Sarah L Becker ◽  
Edna Chiang ◽  
Anna Plantinga ◽  
Hannah V Carey ◽  
Garret Suen ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Gut Microbiota ◽  
Glucose Intolerance ◽  
High Fat Diet ◽  
High Fat ◽  
Low Fat ◽  
Treatment Groups ◽  
Low Fat Diet ◽  
Taxonomic Groups ◽  
Induced Changes

ABSTRACT Artificial sweeteners have been shown to induce glucose intolerance by altering the gut microbiota; however, little is known about the effect of stevia. Here, we investigate whether stevia supplementation induces glucose intolerance by altering the gut microbiota in mice, hypothesizing that stevia would correct high fat diet-induced glucose intolerance and alter the gut microbiota. Mice were split into four treatment groups: low fat, high fat, high fat + saccharin and high fat + stevia. After 10 weeks of treatment, mice consuming a high fat diet (60% kcal from fat) developed glucose intolerance and gained more weight than mice consuming a low fat diet. Stevia supplementation did not impact body weight or glucose intolerance. Differences in species richness and relative abundances of several phyla were observed in low fat groups compared to high fat, stevia and saccharin. We identified two operational taxonomic groups that contributed to differences in beta-diversity between the stevia and saccharin groups: Lactococcus and Akkermansia in females and Lactococcus in males. Our results demonstrate that stevia does not rescue high fat diet-induced changes in glucose tolerance or the microbiota, and that stevia results in similar alterations to the gut microbiota as saccharin when administered in concordance with a high fat diet.

scholarly journals Dietary α-lactalbumin alters energy balance, gut microbiota composition and intestinal nutrient transporter expression in high-fat diet-fed mice

2019 ◽  
Vol 121 (10) ◽  
pp. 1097-1107 ◽  
Author(s):  
Serena Boscaini ◽  
Raul Cabrera-Rubio ◽  
John R. Speakman ◽  
Paul D. Cotter ◽  
John F. Cryan ◽  
...  
Keyword(s):  
Energy Balance ◽  
Gut Microbiota ◽  
Whey Protein ◽  
Energy Intake ◽  
High Fat Diet ◽  
Metabolic Diseases ◽  
Whey Proteins ◽  
Nutrient Transporters ◽  
High Fat ◽  
Cumulative Energy

AbstractRecently there has been a considerable rise in the frequency of metabolic diseases, such as obesity, due to changes in lifestyle and resultant imbalances between energy intake and expenditure. Whey proteins are considered as potentially important components of a dietary solution to the obesity problem. However, the roles of individual whey proteins in energy balance remain poorly understood. This study investigated the effects of a high-fat diet (HFD) containing α-lactalbumin (LAB), a specific whey protein, or the non-whey protein casein (CAS), on energy balance, nutrient transporters expression and enteric microbial populations. C57BL/6J mice (n 8) were given an HFD containing either 20 % CAS or LAB as protein sources or a low-fat diet containing CAS for 10 weeks. HFD-LAB-fed mice showed a significant increase in cumulative energy intake (P=0·043), without differences in body weight, energy expenditure, locomotor activity, RER or subcutaneous and epididymal white adipose tissue weight. HFD-LAB intake led to a decrease in the expression of glut2 in the ileum (P=0·05) and in the fatty acid transporter cd36 (P<0·001) in both ileum and jejunum. This suggests a reduction in absorption efficiency within the small intestine in the HFD-LAB group. DNA from faecal samples was used for 16S rRNA-based assessment of intestinal microbiota populations; the genera Lactobacillus, Parabacteroides and Bifidobacterium were present in significantly higher proportions in the HFD-LAB group. These data indicate a possible functional relationship between gut microbiota, intestinal nutrient transporters and energy balance, with no impact on weight gain.

scholarly journals Sex-dependent hepatic transcripts and metabolites in the development of glucose intolerance and insulin resistance in Zucker diabetic fatty rats

2011 ◽  
Vol 47 (2) ◽  
pp. 129-143 ◽  
Author(s):  
Carolina Gustavsson ◽  
Tomoyoshi Soga ◽  
Erik Wahlström ◽  
Mattias Vesterlund ◽  
Alireza Azimi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Stress Responses ◽  
Female Rats ◽  
Male Rats ◽  
High Fat ◽  
Prediabetic State ◽  
Flight Mass Spectrometry ◽  
Zucker Diabetic Fatty Rats

Male Zucker diabetic fatty (mZDF) rats spontaneously develop type 2 diabetes, whereas females only become diabetic when fed a diabetogenic high-fat diet (high-fat-fed female ZDF rat, HF-fZDF). The aim of this study was to investigate if differences in liver functions could provide clues to this sex difference. Non-diabetic obese fZDF rats were compared with either mZDF or HF-fZDF regarding hepatic molecular profiles, to single out those components that might be protective in the females. High-fat feeding in fZDF led to enhanced weight gain, increased blood glucose and insulin levels, reduced insulin sensitivity and a trend towards reduced glucose tolerance, indicative of a prediabetic state. mZDF rats were diabetic, with low levels of insulin, high levels of glucose, reduced insulin sensitivity and impaired glucose tolerance. Transcript profiling and capillary electrophoresis time-of-flight mass spectrometry were used to indentify hepatic transcripts and metabolites that might be related to this. Many diet-induced alterations in transcript and metabolite levels in female rats were towards a ‘male-like’ phenotype, including reduced lipogenesis, increased fatty acid (FA) oxidation and increased oxidative stress responses. Alterations detected at the level of hepatic metabolites, indicated lower capacity for glutathione (GSH) production in male rats, and higher GSH turnover in females. Taken together, this could be interpreted as if anabolic pathways involving lipogenesis and lipid output might limit the degree of FA oxidation and oxidative stress in female rats. Together with a greater capacity to produce GSH, these hepatic sex differences might contribute to the sex-different development of diabetes in ZDF rats.

scholarly journals Hypothalamic Fkbp51 is induced by fasting, and elevated hypothalamic expression promotes obese phenotypes

2012 ◽  
Vol 302 (8) ◽  
pp. E987-E991 ◽  
Author(s):  
Linda Yang ◽  
Fumiko Isoda ◽  
Kelvin Yen ◽  
Steven P. Kleopoulos ◽  
William Janssen ◽  
...  
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Glucose Tolerance ◽  
Negative Feedback ◽  
High Fat Diet ◽  
High Fat ◽  
Adeno Associated Virus ◽  
Fk506 Binding Protein ◽  
Hypothalamic Nuclei ◽  
Glucocorticoid Action

To discover hypothalamic genes that might play a role in regulating energy balance, we carried out a microarray screen for genes induced by a 48-h fast in male C57Bl/6J mouse hypothalamus. One such gene was Fkbp51 (FK506 binding protein 5; Locus NP_034350). The product of this gene is of interest because it blocks glucocorticoid action, suggesting that fasting-induced elevation of this gene in the hypothalamus may reduce glucocorticoid negative feedback, leading to elevated glucocorticoid levels, thus promoting obese phenotypes. Subsequent analysis demonstrated that a 48-h fast induces Fkbp51 in ventromedial, paraventricular, and arcuate hypothalamic nuclei of mice and rats. To assess if hypothalamic Fkbp51 promotes obesity, the gene was transferred to the hypothalamus via an adeno-associated virus vector. Within 2 wk following Fkbp51 overexpression, mice on a high-fat diet exhibited elevated body weight, without hyperphagia, relative to mice receiving the control mCherry vector. Body weight remained elevated for more than 8 wk and was associated with elevated corticosterone and impaired glucose tolerance. These studies suggest that elevated hypothalamic Fkbp51 promotes obese phenotypes.

scholarly journals Ampicillin-Improved Glucose Tolerance in Diet-Induced Obese C57BL/6NTac Mice Is Age Dependent

2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
I. Rune ◽  
C. H. F. Hansen ◽  
M. Ellekilde ◽  
D. S. Nielsen ◽  
K. Skovgaard ◽  
...  
Keyword(s):  
Dendritic Cell ◽  
Tumor Necrosis Factor ◽  
Glucose Tolerance ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Tumor Necrosis ◽  
Control Group ◽  
High Fat ◽  
Amyloid A ◽  
Necrosis Factor

Ampicillin has been shown to improve glucose tolerance in mice. We hypothesized that this effect is present only if treatment is initiated prior to weaning and that it disappears when treatment is terminated. High-fat fed C57BL/6NTac mice were divided into groups that received Ampicillin at different ages or not at all. We found that both diet and Ampicillin significantly changed the gut microbiota composition in the animals. Furthermore, there was a significant improvement in glucose tolerance in Ampicillin-treated, five-week-old mice compared to nontreated mice in the control group. At study termination, expressions of mRNA coding for tumor necrosis factor, serum amyloid A, and lactase were upregulated, while the expression of tumor necrosis factor (ligand) superfamily member 15 was downregulated in the ileum of Ampicillin-treated mice. Higher dendritic cell percentages were found systemically in high-fat diet mice, and a lower tolerogenic dendritic cell percentage was found both in relation to high-fat diet and late Ampicillin treatment. The results support our hypothesis that a “window” exists early in life in which an alteration of the gut microbiota affects glucose tolerance as well as development of gut immunity and that this window may disappear after weaning.

scholarly journals The Effect of Voluntary Exercise on Gut Microbiota in Partially Hydrolyzed Guar Gum Intake Mice under High-Fat Diet Feeding

Nutrients ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2508
Author(s):  
Takafumi Aoki ◽  
Eri Oyanagi ◽  
Chihiro Watanabe ◽  
Nanako Kobiki ◽  
Suzuka Miura ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Gut Microbiota ◽  
Dietary Fiber ◽  
High Fat Diet ◽  
Guar Gum ◽  
Wheel Running ◽  
Control Diet ◽  
Voluntary Exercise ◽  
High Fat ◽  
Partially Hydrolyzed Guar Gum

Although dietary fiber treatment alters the gut microbiota and its metabolite production, it is unclear whether or not exercise habits can have a supplemental effect on changes in gut microbiota in dietary fiber-treated mice. To clarify the supplemental effect of voluntary exercise on gut microbiota in partially hydrolyzed guar gum (PHGG), which is a soluble dietary fiber, treated mice under high-fat diet (HFD) feeding, 4-week-old male C57BL/6J mice (n = 80) were randomly divided into two dietary groups: the control-diet (CD) and HFD. Then, each dietary group was treated with or without PHGG, and with or without wheel running. After the experimental period, measurement of maximal oxygen consumption, a glucose tolerance test and fecal materials collection for analysis of gut microbiota were carried out. Voluntary exercise load in PHGG treatment under HFD feeding showed the supplemental effect of exercise on obesity (p < 0.01) and glucose tolerance (p < 0.01). Additionally, in both CD and HFD groups, voluntary exercise accelerated the decrease in the Firmicutes/Bacteroidetes ratio in mice fed with PHGG (p < 0.01). These findings suggest that voluntary exercise might activate the prevention of obesity and insulin resistance more via change in gut microbiota in mice administrated with PHGG.

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