scholarly journals Navy Bean Supplementation in Established High-Fat Diet-Induced Obesity Attenuates the Severity of the Obese Inflammatory Phenotype

Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 757
Author(s):  
Jennifer M. Monk ◽  
Wenqing Wu ◽  
Dion Lepp ◽  
K. Peter Pauls ◽  
Lindsay E. Robinson ◽  
...  
Keyword(s):  
Weight Loss ◽  
Control Diet ◽  
Intestinal Health ◽  
High Fat ◽  
Navy Bean ◽  
Fecal Microbiome ◽  
Reduced Body ◽  
Inflammatory Phenotype ◽  
Obesogenic Diet ◽  
Obese Phenotype

Cooked common beans (Phaseolus vulgaris) improve intestinal health in lean mice and attenuate intestinal dysbiosis and inflammation when consumed concurrent with obesity development. We determined the effects of a high-fat (HF) bean supplemented diet in mice with established obesity (induced by 12 weeks of HF diet (60% fat as kcal)) compared to obese mice consuming a HF or low-fat (LF) weight loss control diet. Obese C57BL/6 male mice remained consuming HF for eight weeks or were randomly switched from HF to an isocaloric HF with 15.7% cooked navy bean powder diet (HFàHFB) or LF (11% fat as kcal; HFàLF) (n = 12/group). HFàHFB improved the obese phenotype, including (i) fecal microbiome (increased Prevotella, Akkermansia muciniphila, and short-chain fatty acid levels), (ii) intestinal health (increased ZO-1, claudin-2, Muc2, Relmβ, and Reg3γ expression), and (iii) reduced adipose tissue (AT) inflammatory proteins (NFκBp65, STAT3, IL-6, MCP-1, and MIP-1α), versus HF (p < 0.05). Conversely, HFàLF reduced body weight and circulating hormones (leptin, resistin, and PAI-1) versus HF and HFàHFB (p < 0.05); however, AT inflammation and intestinal health markers were not improved to the same degree as HFàHFB (p < 0.05). Despite remaining on a HF obesogenic diet, introducing beans in established obesity improved the obese phenotype (intestinal health and adipose inflammation) more substantially than weight loss alone.

Supplementation with methyl donors during lactation to high-fat-sucrose-fed dams protects offspring against liver fat accumulation when consuming an obesogenic diet

2014 ◽  
Vol 5 (5) ◽  
pp. 385-395 ◽  
Author(s):  
P. Cordero ◽  
F. I. Milagro ◽  
J. Campion ◽  
J. A. Martinez
Keyword(s):  
Control Diet ◽  
Liver Fat ◽  
Chow Diet ◽  
Mrna Levels ◽  
High Fat ◽  
Adult Rats ◽  
Fat Accumulation ◽  
Methyl Donors ◽  
Methyl Donor ◽  
Obesogenic Diet

Methyl donor supplementation has been reported to prevent obesity-induced liver fat accumulation in adult rats. We hypothesized that this protection could be mediated by perinatal nutrition. For this purpose, we assessed the response to an obesogenic diet (high-fat-sucrose, HFS) during adulthood depending on maternal diet during lactation. Female Wistar rats fed control diet during pregnancy were assigned to four postpartum dietary groups: control, control supplemented with methyl donors (choline, betaine, folic acid, vitamin B12), HFS and HFS supplemented with methyl donors. At weaning, the male offspring was transferred to a chow diet and at week 12th assigned to a control or a HFS diet during 8 weeks. The offspring whose mothers were fed HFS during lactation showed increased adiposity (19%,P<0.001). When fed the HFS diet as adults, offspring whose mothers were HFS supplemented had more body fat (23%,P<0.001) than those from HFS non-supplemented. However, they showed lower liver fat accumulation (−18%,P<0.001). Srebf1, Dnmt1 and Lepr liver mRNA levels increased after adulthood HFS feeding. In those animals HFS fed during adulthood, previous maternal HFS decreased Lepr and Dnmt1 expression levels when compared with c-HFS offspring, while the supplementation of control and HFS-fed dams, respectively, induced higher hepatic Mme and Lepr mRNA levels after adult HFS intake compared with hfs-HFS offspring. In conclusion, maternal HFS diet during lactation influenced the response to an obesogenic diet in the adult progeny. Interestingly, dietary methyl donor supplementation in lactating mothers fed an obesogenic diet reduced liver fat accumulation, but increased adipose tissue storage in adult HFS-fed offspring.

High-fat diet induces site-specific unresponsiveness to LPS-stimulated STAT3 activation in the hypothalamus

2014 ◽  
Vol 306 (1) ◽  
pp. R34-R44 ◽  
Author(s):  
Beatriz de Carvalho Borges ◽  
Rodrigo Rorato ◽  
Ernane Torres Uchoa ◽  
Paula Marangon ◽  
Glauber S. F. da Silva ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Food Intake ◽  
Energy Expenditure ◽  
Brain Stem ◽  
High Fat Diet ◽  
Control Diet ◽  
Body Weight Loss ◽  
Hypothalamic Nucleus ◽  
High Fat

Hypophagia induced by inflammation is associated with Janus kinase (JAK)-2/signal transducer and activator of transcription (STAT) 3 signaling pathway, and leptin-mediated hypophagia is also mediated by JAK2-STAT3 pathway. We have previously reported that lipopolysaccharide (LPS) did not reduce food intake in leptin-resistant high-fat diet (HFD) rats but maintained body weight loss. We investigated whether changes in p-STAT3 expression in the hypothalamus and brain stem could account for the desensitization of hypophagia in HFD animals after a low LPS dose (100 μg/kg). Wistar rats fed standard diet (3.95 kcal/g) or HFD (6.3 kcal/g) for 8 wk were assigned into control diet-saline, control diet-LPS, HFD-saline, and HFD-LPS groups. LPS reduced feeding in the control diet but not HFD. This group showed no p-STAT3 expression in the paraventricular nucleus (PVN) and ventromedial hypothalamic nucleus (VMH), but sustained, though lower than control, p-STAT3 in the nucleus of the solitary tract (NTS) and raphe pallidus (RPa). LPS decreased body weight in HFD rats and increased Fos expression in the NTS. LPS increased body temperature, oxygen consumption, and energy expenditure in both control diet and HFD rats, and this response was more pronounced in HFD-LPS group. Brown adipose tissue (BAT) thermogenesis and increased energy expenditure seem to contribute to body weight loss in HFD-LPS. This response might be related with increased brain stem activation. In conclusion, LPS activates STAT3-mediated pathway in the hypothalamus and brain stem, leading to hypophagia, however, LPS effects on food intake, but not body weight loss, are abolished by leptin resistance induced by HFD. The preserved STAT3 phosphorylation in the brain stem suggests that unresponsiveness to LPS on STAT3 activation under HFD might be selective to the hypothalamus.

scholarly journals Prebiotic milk oligosaccharides prevent development of obese phenotype, impairment of gut permeability, and microbial dysbiosis in high fat-fed mice

2017 ◽  
Vol 312 (5) ◽  
pp. G474-G487 ◽  
Author(s):  
M. Kristina Hamilton ◽  
Charlotte C. Ronveaux ◽  
Bret M. Rust ◽  
John W. Newman ◽  
Melissa Hawley ◽  
...  
Keyword(s):  
Weight Gain ◽  
Gut Microbiota ◽  
Intestinal Permeability ◽  
Control Diet ◽  
Bovine Milk ◽  
High Fat ◽  
Milk Oligosaccharides ◽  
Microbial Dysbiosis ◽  
Diet Induced Obesity ◽  
Obese Phenotype

Microbial dysbiosis and increased intestinal permeability are targets for prevention or reversal of weight gain in high-fat (HF) diet-induced obesity (DIO). Prebiotic milk oligosaccharides (MO) have been shown to benefit the host intestine but have not been used in DIO. We hypothesized that supplementation with bovine MO would prevent the deleterious effect of HF diet on the gut microbiota and intestinal permeability and attenuate development of the obese phenotype. C57BL/6 mice were fed a control diet, HF (40% fat/kcal), or HF + prebiotic [6%/kg bovine milk oligosaccharides (BMO) or inulin] for 1, 3, or 6 wk. Gut microbiota and intestinal permeability were assessed in the ileum, cecum, and colon. Addition of BMO to the HF diet significantly attenuated weight gain, decreased adiposity, and decreased caloric intake; inulin supplementation also lowered weight gain and adiposity, but this did not reach significance. BMO and inulin completely abolished the HF diet-induced increase in paracellular and transcellular permeability in the small and large intestine. Both BMO and inulin increased abundance of beneficial microbes Bifidobacterium and Lactobacillus in the ileum. However, inulin supplementation altered phylogenetic diversity and decreased species richness. We conclude that addition of BMO to the HF diet completely prevented increases in intestinal permeability and microbial dysbiosis and was partially effective to prevent weight gain in DIO. NEW & NOTEWORTHY This study provides the first report of the effects of prebiotic bovine milk oligosaccharides on the host phenotype of high-fat diet-induced obesity in mice.

Effect of repeated stress on body weight and body composition of rats fed low- and high-fat diets

1998 ◽  
Vol 275 (6) ◽  
pp. R1928-R1938 ◽  
Author(s):  
Ruth B. S. Harris ◽  
Jun Zhou ◽  
Bradley D. Youngblood ◽  
Igor I. Rybkin ◽  
Gennady N. Smagin ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Food Intake ◽  
High Fat Diet ◽  
Corn Oil ◽  
Coconut Oil ◽  
High Fat ◽  
Adult Rats ◽  
Reduced Body ◽  
Fat Diets

Exposure to the moderate stressor of 3-h restraint for 3 consecutive days causes a temporary drop in food intake but a permanent reduction in body weight in adult rats. Young rats did not show the same response. Food intake of adult rats exposed to repeated restraint was significantly lower than that of controls for 4 days after the end of stress, and there was no rebound hyperphagia. Body weight remained significantly lower for at least 40 days after stress. When the rats were fed a high-fat diet of 80% chow and 20% vegetable shortening (48% kcal fat, 16% protein), lean body mass accounted for all of the weight loss in stressed rats. When the experiment was repeated with a purified high-fat diet containing corn oil and coconut oil as the source of fat (41% kcal fat, 16% protein), weight loss consisted of both lean and fat tissue. There were no sustained changes in single time point measures of corticosterone, insulin, or leptin that could account for the reduced body weight in these rats.

scholarly journals Weight Loss in Response to Food Deprivation Predicts The Extent of Diet Induced Obesity in C57BL/6J Mice

2014 ◽  
Author(s):  
Matthew J. Peloqiun ◽  
Dave Bridges
Keyword(s):  
Weight Loss ◽  
Weight Gain ◽  
Food Deprivation ◽  
High Fat Diet ◽  
Control Diet ◽  
Chow Diet ◽  
High Fat ◽  
Strong Negative Correlation ◽  
Diet Induced Obesity ◽  
Serum Hormone

Inbred C57BL/6J mice have been used to study diet-induced obesity and the detrimental physiological effects associated with it. Little is understood about predictive factors that predispose an animal to weight gain. To address this, mice were fed a high fat diet, control diet or normal chow diet. Several measurements including pre-diet serum hormone levels and pre-diet body weight were analyzed, but these had limited predictive value regarding weight gain. However, baseline measurements of weight loss in response to food deprivation showed a strong negative correlation with high fat diet-induced weight gain. These data suggest that fasting-induced weight loss in adolescent mice is a useful predictor of diet-induced weight gain.

scholarly journals Prenatal Choline Supplementation during High-Fat Feeding Improves Long-Term Blood Glucose Control in Male Mouse Offspring

Nutrients ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 144
Author(s):  
Hunter W. Korsmo ◽  
Kaydine Edwards ◽  
Bhoomi Dave ◽  
Chauntelle Jack-Roberts ◽  
Huanling Yu ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Maternal Obesity ◽  
Control Diet ◽  
Blood Glucose Control ◽  
Female Offspring ◽  
Male Offspring ◽  
High Fat ◽  
Obesogenic Diet ◽  
Dietary Treatments

Maternal obesity increases the risk of metabolic dysregulation in rodent offspring, especially when offspring are exposed to a high-fat (HF), obesogenic diet later in life. We previously demonstrated that maternal choline supplementation (MCS) in HF-fed mouse dams during gestation prevents fetal overgrowth and excess adiposity. In this study, we examined the long-term metabolic influence of MCS. C57BL/6J mice were fed a HF diet with or without choline supplementation prior to and during gestation. After weaning, their pups were exposed to either a HF or control diet for 6 weeks before measurements. Prenatal and post-weaning dietary treatments led to sexually dimorphic responses. In male offspring, while post-weaning HF led to impaired fasting glucose and worse glucose tolerance (p < 0.05), MCS in HF dams (HFCS) attenuated these changes. HFCS (versus maternal normal fat control) appeared to improve metabolic functioning of visceral adipose tissue during post-weaning HF feeding, preventing the elevation in leptin and increasing (p < 0.05) mRNA expression of insulin receptor substrate 1 (Irs1) that promotes peripheral insulin signaling in male offspring. In contrast, MCS had minimal effects on metabolic outcomes of female offspring. In conclusion, MCS during HF feeding in mice improves long-term blood glucose homeostasis in male offspring when they are faced with a postnatal obesogenic environment.

scholarly journals Effects of Edible Insect Tenebrio molitor Larva Fermentation Extract as a Substitute Protein on Hepatosteatogenesis and Proteomic Changes in Obese Mice Induced by High-Fat Diet

2021 ◽  
Vol 22 (7) ◽  
pp. 3615
Author(s):  
Ju Ri Ham ◽  
Ra-Yeong Choi ◽  
Yongjin Lee ◽  
Mi-Kyung Lee
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Control Diet ◽  
Tenebrio Molitor ◽  
High Fat ◽  
Edible Insect ◽  
Reduced Body ◽  
Protein Rich

Mealworms (Tenebrio molitor larva) are an edible insect and a protein-rich food; however, research on mealworms as a substitute protein is insufficient. In this study, mealworm fermentation extract (TMP) was assessed as a replacement for soy protein (SP) in a control diet (CON) or a high-fat diet (HFD) of mice for 12 weeks. TMP substitution reduced body weight, body weight gain, body fat mass (perirenal and mesenteric), fat size, glucose intolerance, and insulin resistance compared to the HFD-SP group. TMP alleviated hepatic steatosis (lipid contents and lipid droplets) in high-fat-fed mice and down-regulated the PPARγ, CD36, and DGAT2 gene levels. Proteomic analysis showed that a HFD for 12 weeks up-regulated 20 proteins and down-regulated 17 proteins in mice fed SP. On the other hand, TMP reversed the protein profiles. TMP significantly down-regulated KHK, GLO1, ATP5H, SOD, and DDAH1 and up-regulated DLD, Mup1, CPS1, Ces3b, PDI, and HYOU1 compared to the HFD-SP group. These proteins are involved in the glucose, lipid, and amino acid metabolism, as well as in oxidative stress and endoplasmic reticulum stress. Thus, substituting SP for TMP helped improve HFD-induced obesity, steatosis, and insulin resistance in mice. These results suggest that TMP is a potential substitute for commonly used protein sources.

scholarly journals AB-Kefir Reduced Body Weight and Ameliorated Inflammation in Adipose Tissue of Obese Mice Fed a High-Fat Diet, but Not a High-Sucrose Diet

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2182
Author(s):  
Yung-Tsung Chen ◽  
Ai-Hua Hsu ◽  
Shiou-Yun Chiou ◽  
Yu-Chun Lin ◽  
Jin-Seng Lin
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Control Diet ◽  
Liver Weight ◽  
High Fat ◽  
Reduced Body ◽  
Different Types

Consumption of different types of high-calorie foods leads to the development of various metabolic disorders. However, the effects of multi-strain probiotics on different types of diet-induced obesity and intestinal dysbiosis remain unclear. In this study, mice were fed a control diet, high-fat diet (HFD; 60% kcal fat and 20% kcal carbohydrate), or western diet (WD; 40% kcal fat and 43% kcal carbohydrate) and administered with multi-strain AB-Kefir containing six strains of lactic acid bacteria and a Bifidobacterium strain, at 109 CFU per mouse for 10 weeks. Results demonstrated that AB-Kefir reduced body weight gain, glucose intolerance, and hepatic steatosis with a minor influence on gut microbiota composition in HFD-fed mice, but not in WD-fed mice. In addition, AB-Kefir significantly reduced the weight and size of adipose tissues by regulating the expression of CD36, Igf1, and Pgc1 in HFD-fed mice. Although AB-Kefir did not reduce the volume of white adipose tissue, it markedly regulated CD36, Dgat1 and Mogat1 mRNA expression. Moreover, the abundance of Eubacterium_coprostanoligenes_group and Ruminiclostridium significantly correlated with changes in body weight, liver weight, and fasting glucose in test mice. Overall, this study provides important evidence to understand the interactions between probiotics, gut microbiota, and diet in obesity treatment.

scholarly journals Adverse effects of obesity and/or high-fat diet on oocyte quality and metabolism are not reversible with resumption of regular diet in mice

2015 ◽  
Vol 27 (4) ◽  
pp. 716 ◽  
Author(s):  
Kasey A. Reynolds ◽  
Anna L. Boudoures ◽  
Maggie M.-Y. Chi ◽  
Qiang Wang ◽  
Kelle H. Moley
Keyword(s):  
Adverse Effects ◽  
High Fat Diet ◽  
Control Diet ◽  
Intervention Group ◽  
Oocyte Quality ◽  
Metabolic Parameters ◽  
Control Group ◽  
Obese Women ◽  
High Fat ◽  
Obesogenic Diet

Obesity adversely affects reproduction and results in oocyte defects in both mice and humans. In the present study we used a mouse model to examine whether the adverse effects of an obesogenic diet on oocyte metabolism and morphology can be reversed by return to a control diet. The intervention group consisted of C57BL6/J mice placed on a high-fat diet (HFD; 35.8% fat and 20.2% protein by nutritional content) for 6 weeks and then switched to an isocaloric control diet (CD; 13% fat and 25% protein) for 8 weeks (HFD/CD mice). The control group consisted of age-matched C57BL6/J mice maintained on CD for 14 weeks (CD/CD mice). Although metabolic parameters (weight, glucose tolerance and cholesterol levels) of HFD/CD mice returned to normal after this ‘diet reversal’ period, several oocyte defects were not reversible. These HFD/CD oocytes demonstrated significantly higher percentages of abnormal meiotic spindles, lower mitochondrial membrane potential and lower ATP and citrate levels, and higher percentages of abnormal lipid accumulation and mitochondrial distribution compared with CD/CD mice. These results suggest that the negative effects of an obesogenic diet on oocyte quality are not reversible, despite reversal of metabolic parameters. These data may provide better insight when counselling obese women regarding reproductive options and success.

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