scholarly journals High-Fat Diet and Age-Dependent Effects of IgA-Bearing Cell Populations in the Small Intestinal Lamina Propria in Mice

2021 ◽  
Vol 22 (3) ◽  
pp. 1165
Author(s):  
Yuta Sakamoto ◽  
Masatoshi Niwa ◽  
Ken Muramatsu ◽  
Satoshi Shimo
Keyword(s):  
Immune Function ◽  
Lamina Propria ◽  
High Fat Diet ◽  
Immunoglobulin A ◽  
Immune Functions ◽  
High Fat ◽  
Intestinal Villi ◽  
Diet Induced Obesity ◽  
Obesity And Diabetes

Several studies highlighted that obesity and diabetes reduce immune function. However, changes in the distribution of immunoglobins (Igs), including immunoglobulin-A (IgA), that have an important function in mucosal immunity in the intestinal tract, are unclear. This study aimed to investigate the impaired immune functions in the context of a diet-induced obese murine model via the assessment of the Igs in the intestinal villi. We used mice fed a high-fat diet (HFD) from four to 12 or 20 weeks of age. The distributions of IgA, IgM, and IgG1 were observed by immunohistochemistry. Interestingly, we observed that IgA was immunolocalized in many cells of the lamina propria and that immunopositive cells increased in mice aged 12 to 20 weeks. Notably, mice fed HFD showed a reduced number of IgA-immunopositive cells in the intestinal villi compared to those fed standard chow. Of note, the levels of IgM and IgG1 were also reduced in HFD fed mice. These results provide insights into the impaired mucosal immune function arising from diet-induced obesity and type 2 diabetes.

scholarly journals Evaluation of voglibose on body weight in rats

2019 ◽  
Vol 8 (6) ◽  
pp. 1159
Author(s):  
Sarita Mulkalwar ◽  
Tanya Gupta ◽  
Vishwanath Kulkarni ◽  
A. V. Tilak ◽  
B. T. Rane ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Body Weight ◽  
High Fat Diet ◽  
Normal Diet ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Obesity Drugs

Background: As of 2018, 2.1 billion people nearly 30% of the world’s population are either obese or overweight. Worldwide obesity has nearly tripled since 1975. It is an emerging health problem with major adverse effects on health. It is a risk factor for many chronic diseases but is best known for its role in metabolic syndrome, which can lead to type 2 diabetes mellitus as well as cardiovascular diseases. Anti-obesity drugs are available but have many side effects. Voglibose, an antidiabetic drug, is an alpha glucosidase inhibitor which shows promising results in the reduction of body weight with minimal side effects.Methods: Voglibose (7 mg/kg) was administered to rats fed with normal laboratory chows and high fat diet to see its effect on body weight, body mass index, abdominal and thoracic circumference, and lipid profile at the end of 12 weeks.Results: Administration of voglibose significantly reduced food consumption, feed efficiency and increase in body weight induced by high fat diet in rats. Rats fed on normal diet also showed reductions in the same parameters, suggesting its weight lowering effect. Reductions in the anthropometric measurements, hypolipidemic effects and glucose lowering effects were also observed.Conclusions: Voglibose prevented high fat diet-induced obesity and improvement in metabolic profile, which ultimately has systemic effects on body weight in rats. Further studies are needed to see its potential therapeutic use in obese patients with type 2 diabetes mellitus, and related complications.

New Prebiotics to Ameliorate High-Fat Diet-Induced Obesity and Diabetes via Modulation of Microbiome-Gut-Brain Axis

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 264-LB ◽  
Author(s):  
SHOKOUH AHMADI ◽  
RAVINDER K. NAGPAL ◽  
SHAOHUA WANG ◽  
HARIOM YADAV
Keyword(s):  
High Fat Diet ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Obesity And Diabetes

scholarly journals Inhibition of ADRP prevents diet-induced insulin resistance

2008 ◽  
Vol 295 (3) ◽  
pp. G621-G628 ◽  
Author(s):  
Gladys M. Varela ◽  
Daniel A. Antwi ◽  
Ravindra Dhir ◽  
Xiaoyan Yin ◽  
Neel S. Singhal ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
High Fat Diet ◽  
Insulin Action ◽  
Fatty Acyl ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Tracer Techniques ◽  
Adipose Differentiation ◽  
Lipid Droplet Protein

Diets with high fat content induce steatosis, insulin resistance, and type 2 diabetes. The lipid droplet protein adipose differentiation-related protein (ADRP) mediates hepatic steatosis, but whether this affects insulin action in the liver or peripheral organs in diet-induced obesity is uncertain. We fed C57BL/6J mice a high-fat diet and simultaneously treated them with an antisense oligonucleotide (ASO) against ADRP for 4 wk. Glucose homeostasis was assessed with clamp and tracer techniques. ADRP ASO decreased the levels of triglycerides and diacylglycerol in the liver, but fatty acids, long-chain fatty acyl CoAs, ceramides, and cholesterol were unchanged. Insulin action in the liver was enhanced after ADRP ASO treatment, whereas muscle and adipose tissue were not affected. ADRP ASO increased the phosphorylation of insulin receptor substrate (IRS)1, IRS2, and Akt, and decreased gluconeogenic enzymes and PKCε, consistent with its insulin-sensitizing action. These results demonstrate an important role for ADRP in the pathogenesis of diet-induced insulin resistance.

scholarly journals Consumption of Curcumin Elevates Fecal Immunoglobulin A, an Index of Intestinal Immune Function, in Rats Fed a High-Fat Diet

2010 ◽  
Vol 56 (1) ◽  
pp. 68-71 ◽  
Author(s):  
Yukako OKAZAKI ◽  
Yunkyung HAN ◽  
Mai KAYAHARA ◽  
Toshiro WATANABE ◽  
Hirofumi ARISHIGE ◽  
...  
Keyword(s):  
Immune Function ◽  
High Fat Diet ◽  
Immunoglobulin A ◽  
High Fat

scholarly journals Role of Muscle c-Jun NH2-Terminal Kinase 1 in Obesity-Induced Insulin Resistance

2009 ◽  
Vol 30 (1) ◽  
pp. 106-115 ◽  
Author(s):  
Guadalupe Sabio ◽  
Norman J. Kennedy ◽  
Julie Cavanagh-Kyros ◽  
Dae Young Jung ◽  
Hwi Jin Ko ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
High Fat Diet ◽  
Wild Type ◽  
High Fat ◽  
Akt Activation ◽  
Peripheral Insulin Resistance ◽  
Diet Induced Obesity

ABSTRACT Obesity caused by feeding of a high-fat diet (HFD) is associated with an increased activation of c-Jun NH2-terminal kinase 1 (JNK1). Activated JNK1 is implicated in the mechanism of obesity-induced insulin resistance and the development of metabolic syndrome and type 2 diabetes. Significantly, Jnk1 − / − mice are protected against HFD-induced obesity and insulin resistance. Here we show that an ablation of the Jnk1 gene in skeletal muscle does not influence HFD-induced obesity. However, muscle-specific JNK1-deficient (MKO) mice exhibit improved insulin sensitivity compared with control wild-type (MWT) mice. Thus, insulin-stimulated AKT activation is suppressed in muscle, liver, and adipose tissue of HFD-fed MWT mice but is suppressed only in the liver and adipose tissue of MKO mice. These data demonstrate that JNK1 in muscle contributes to peripheral insulin resistance in response to diet-induced obesity.

scholarly journals Autophagy is involved in adipogenic differentiation by repressesing proteasome-dependent PPARγ2 degradation

2013 ◽  
Vol 305 (4) ◽  
pp. E530-E539 ◽  
Author(s):  
Chongben Zhang ◽  
Yingke He ◽  
Mitsuhara Okutsu ◽  
Lai Chun Ong ◽  
Yi Jin ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Animal Studies ◽  
Adipogenic Differentiation ◽  
Daily Injection ◽  
Related Gene ◽  
High Fat ◽  
Pharmacological Interventions ◽  
Diet Induced Obesity

Animal studies have shown that autophagy is essential in the process of obesity. Here, we performed daily injection of the autophagy inhibitor chloroquine (CQ) in mice and found that systemic administration of CQ blocks high-fat diet-induced obesity. To investigate the potential underlying molecular mechanism, we employed genetic and pharmacological interventions in cultured preadipocytes to investigate the role of autophagy in the control of the expression of the adipogenic regulator peroxisome proliferatior-activated receptor-γ (PPARγ). We show that adipogenic differentiation of 3T3-L1 preadipocytes is associated with activation of autophagy and increased PPARγ2 protein level. Treatment with CQ, shRNA-mediated knockdown, or genetic engineering-induced deletion of autophagy-related gene 5 (Atg5) promoted proteasome-dependent PPARγ2 degradation and attenuated adipogenic differentiation. Therefore, activated autophagy increases PPARγ2 stability and promotes adipogenic differentiation, and inhibition of autophagy may prevent high-fat diet-induced obesity and the consequential type 2 diabetes.

scholarly journals Changes in Gut Microbiota Control Metabolic Endotoxemia-Induced Inflammation in High-Fat Diet-Induced Obesity and Diabetes in Mice

Diabetes ◽  
2008 ◽  
Vol 57 (6) ◽  
pp. 1470-1481 ◽  
Author(s):  
P. D. Cani ◽  
R. Bibiloni ◽  
C. Knauf ◽  
A. Waget ◽  
A. M. Neyrinck ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
High Fat Diet ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Diabetes In Mice ◽  
Obesity And Diabetes ◽  
Metabolic Endotoxemia

scholarly journals RGC32 deficiency protects against high-fat diet-induced obesity and insulin resistance in mice

2014 ◽  
Vol 224 (2) ◽  
pp. 127-137 ◽  
Author(s):  
Xiao-Bing Cui ◽  
Jun-Na Luan ◽  
Jianping Ye ◽  
Shi-You Chen
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
High Fat Diet ◽  
Tolerance Test ◽  
High Fat ◽  
Diet Induced Obesity

Obesity is an important independent risk factor for type 2 diabetes, cardiovascular diseases and many other chronic diseases. Adipose tissue inflammation is a critical link between obesity and insulin resistance and type 2 diabetes and a contributor to disease susceptibility and progression. The objective of this study was to determine the role of response gene to complement 32 (RGC32) in the development of obesity and insulin resistance. WT and RGC32 knockout (Rgc32−/− (Rgcc)) mice were fed normal chow or high-fat diet (HFD) for 12 weeks. Metabolic, biochemical, and histologic analyses were performed. 3T3-L1 preadipocytes were used to study the role of RGC32 in adipocytes in vitro. Rgc32−/− mice fed with HFD exhibited a lean phenotype with reduced epididymal fat weight compared with WT controls. Blood biochemical analysis and insulin tolerance test showed that RGC32 deficiency improved HFD-induced dyslipidemia and insulin resistance. Although it had no effect on adipocyte differentiation, RGC32 deficiency ameliorated adipose tissue and systemic inflammation. Moreover, Rgc32−/− induced browning of adipose tissues and increased energy expenditure. Our data indicated that RGC32 plays an important role in diet-induced obesity and insulin resistance, and thus it may serve as a potential novel drug target for developing therapeutics to treat obesity and metabolic disorders.

Sign in / Sign up

Export Citation Format

Share Document