scholarly journals Combined Soluble Fiber-Mediated Intestinal Microbiota Improve Insulin Sensitivity of Obese Mice

Nutrients ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 351 ◽  
Author(s):  
Chuanhui Xu ◽  
Jianhua Liu ◽  
Jianwei Gao ◽  
Xiaoyu Wu ◽  
Chenbin Cui ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Dietary Fiber ◽  
Intestinal Microbiota ◽  
Binding Capacity ◽  
Basal Diet ◽  
Short Chain Fatty Acids ◽  
Obese Mice ◽  
Soluble Fiber ◽  
Water Binding

Dietary fiber, an important regulator of intestinal microbiota, is a promising tool for preventing obesity and related metabolic disorders. However, the functional links between dietary fiber, intestinal microbiota, and obesity phenotype are still not fully understood. Combined soluble fiber (CSF) is a synthetic mixture of polysaccharides and displays high viscosity, water-binding capacity, swelling capacity, and fermentability. We found that supplementing high-fat diet (HFD) with 6% CSF significantly improved the insulin sensitivity of obese mice without affecting their body weight. Replacing the HFD with normal chow basal diet (NCD), the presence of CSF in the feed significantly enhanced satiety, decreased energy intake, promoted weight and fat loss, and augmented insulin sensitivity. CSF also improved the intestinal morphological integrity, attenuated systemic inflammation, promoted intestinal microbiota homeostasis, and stabilized the production of short-chain fatty acids (SCFAs) that was perturbed during HFD-induced obesity, and these stabilizing effects were more prominent when the basal diet was switched to NCD. The enrichment of bacteria of the S24-7 family and Allobaculum genus increased markedly in the intestine following 6% CSF supplementation- and correlated with decreased adiposity and insulin resistance. Five bacterial genera that were decreased by CSF, including Oscillospira, unclassified Lachonospitaceae, unclassified Clostridiales, unclassified Desulfovibrionaceae, and unclassified Ruminococcae, were subjected to co-occurrence network analysis and were positively correlated to adiposity and insulin resistance, indicating a key role in the microbial response to CSF. Thus, CSF has a potential to promote insulin sensitivity and even reduce obesity via beneficial regulation of the gut microecosystem.

Transthyretin contributes to insulin resistance and diminishes exercise-induced insulin sensitivity in obese mice by inhibiting AMPK activity in skeletal muscle

2021 ◽  
Author(s):  
Yingzi He ◽  
Ruojun Qiu ◽  
Beibei Wu ◽  
Weiwei Gui ◽  
Xihua Lin ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Inhibitory Effect ◽  
Quadriceps Femoris ◽  
Treadmill Training ◽  
C2c12 Cells ◽  
Obese Mice ◽  
Insulin Resistant ◽  
Ampk Activity ◽  
Exercise Induced

Exercise improves obesity-induced insulin resistance and metabolic disorders via mechanisms that remain unclear. Here, we show that the levels of the hepatokine transthyretin (TTR) in circulation are elevated in insulin-resistant individuals including high-fat diet (HFD)-induced obese mice, db/db mice, and patients with metabolic syndrome. Liver Ttr mRNA and circulating TTR levels were reduced in mice by treadmill training, as was the TTR levels in quadriceps femoris muscle; however, AMPK signalling activity was enhanced. Transgenic overexpression of TTR or injection of purified TTR triggered insulin resistance in mice fed on regular chow (RC). Furthermore, TTR overexpression reduced the beneficial effects of exercise on insulin sensitivity in HFD-fed mice. TTR was internalized by muscle cells via the membrane receptor Grp78 and the internalization into the quadriceps femoris was reduced by treadmill training. The TTR/Grp78 combination in C2C12 cells was increased, whereas the AMPK activity of C2C12 cells was decreased as the TTR concentration rose. Additionally, Grp78 silencing prevented the TTR internalization and reversed its inhibitory effect on AMPK activity in C2C12 cells. Our study suggests that elevated circulating TTR may contribute to insulin resistance and counteract the exercise-induced insulin sensitivity improvement; the TTR suppression might be an adaptive response to exercise through enhancing AMPK activity in skeletal muscles.

scholarly journals Soluble Fiber with High Water-Binding Capacity, Swelling Capacity, and Fermentability Reduces Food Intake by Promoting Satiety Rather Than Satiation in Rats

Nutrients ◽  
2016 ◽  
Vol 8 (10) ◽  
pp. 615 ◽  
Author(s):  
Chengquan Tan ◽  
Hongkui Wei ◽  
Xichen Zhao ◽  
Chuanhui Xu ◽  
Yuanfei Zhou ◽  
...  
Keyword(s):  
Food Intake ◽  
Binding Capacity ◽  
High Water ◽  
Soluble Fiber ◽  
Water Binding ◽  
Swelling Capacity

scholarly journals CaMKIV limits metabolic damage through induction of hepatic autophagy by CREB in obese mice

2020 ◽  
Vol 244 (2) ◽  
pp. 353-367 ◽  
Author(s):  
Jiali Liu ◽  
Yue Li ◽  
Xiaoyan Zhou ◽  
Xi Zhang ◽  
Hao Meng ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Inflammatory Response ◽  
Mitochondrial Dysfunction ◽  
High Fat Diet ◽  
Insulin Action ◽  
Hepatic Insulin Resistance ◽  
Obese Mice ◽  
High Fat ◽  
Impaired Insulin

High-fat diet (HFD) not only induces insulin resistance in liver, but also causes autophagic imbalance and metabolic disorders, increases chronic inflammatory response and induces mitochondrial dysfunction. Calcium/calmodulin-dependent protein kinase IV (CaMKIV) has recently emerged as an important regulator of glucose metabolism and skeletal muscle insulin action. Its activation has been involved in the improvement of hepatic and adipose insulin action. But the underlying mechanism is not fully understood. In the present study, we aimed to address the direct effects of CaMKIV in vivo and to evaluate the potential interaction of impaired insulin sensitivity and autophagic disorders in hepatic insulin resistance. Our results indicated obese mice receiving CaMKIV showed decreased blood glucose and serum insulin and improved insulin sensitivity as well as increased glucose tolerance compared with vehicle injection. Meanwhile, defective hepatic autophagy activity, impaired insulin signaling, increased inflammatory response and mitochondrial dysfunction in liver tissues which are induced by high-fat diet were also effectively alleviated by injection of CaMKIV. Consistent with these results, the addition of CaMKIV to the culture medium of BNL cl.2 hepatocytes markedly restored palmitate-induced hepatic insulin resistance and autophagic imbalance. These effects were nullified by blockade of cyclic AMP response element-binding protein (CREB), indicating the causative role of CREB in action of CaMKIV. Our findings suggested that CaMKIV restores hepatic autophagic imbalance and improves impaired insulin sensitivity via phosphorylated CREB signaling pathway, which may offer novel opportunities for treatment of obesity and diabetes.

scholarly journals Adipocyte PU.1 knockout promotes insulin sensitivity in HFD-fed obese mice

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Denise E. Lackey ◽  
Felipe C. G. Reis ◽  
Roi Isaac ◽  
Rizaldy C. Zapata ◽  
Dalila El Ouarrat ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Target Genes ◽  
Obese Mice ◽  
Tissue Macrophage

Abstract Insulin resistance is a key feature of obesity and type 2 diabetes. PU.1 is a master transcription factor predominantly expressed in macrophages but after HFD feeding PU.1 expression is also significantly increased in adipocytes. We generated adipocyte specific PU.1 knockout mice using adiponectin cre to investigate the role of PU.1 in adipocyte biology, insulin and glucose homeostasis. In HFD-fed obese mice systemic glucose tolerance and insulin sensitivity were improved in PU.1 AKO mice and clamp studies indicated improvements in both adipose and liver insulin sensitivity. At the level of adipose tissue, macrophage infiltration and inflammation was decreased and glucose uptake was increased in PU.1 AKO mice compared with controls. While PU.1 deletion in adipocytes did not affect the gene expression of PPARg itself, we observed increased expression of PPARg target genes in eWAT from HFD fed PU.1 AKO mice compared with controls. Furthermore, we observed decreased phosphorylation at serine 273 in PU.1 AKO mice compared with fl/fl controls, indicating that PPARg is more active when PU.1 expression is reduced in adipocytes. Therefore, in obesity the increased expression of PU.1 in adipocytes modifies the adipocyte PPARg cistrome resulting in impaired glucose tolerance and insulin sensitivity.

scholarly journals Selenoprotein W deficiency does not affect oxidative stress and insulin sensitivity in the skeletal muscle of high-fat diet-fed obese mice

2019 ◽  
Vol 317 (6) ◽  
pp. C1172-C1182 ◽  
Author(s):  
Min-Gyeong Shin ◽  
Hye-Na Cha ◽  
Soyoung Park ◽  
Yong-Woon Kim ◽  
Jong-Yeon Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
High Fat Diet ◽  
Control Diet ◽  
In Vivo Studies ◽  
Selenoprotein W ◽  
Obese Mice ◽  
High Fat

Selenoprotein W (SelW) is a selenium-containing protein with a redox motif found abundantly in the skeletal muscle of rodents. Previous in vitro studies suggest that SelW plays an antioxidant role; however, relatively few in vivo studies have addressed the antioxidant role of SelW. Since oxidative stress is a causative factor for the development of insulin resistance in obese subjects, we hypothesized that if SelW plays a role as an antioxidant, SelW deficiency could aggravate the oxidative stress and insulin resistance caused by a high-fat diet. SelW deficiency did not affect insulin sensitivity and H2O2 levels in the skeletal muscle of control diet-fed mice. SelW levels in the skeletal muscle were decreased by high-fat diet feeding for 12 wk. High-fat diet induced obesity and insulin resistance and increased the levels of H2O2 and oxidative stress makers, which were not affected by SelW deficiency. High-fat diet feeding increased the expression of antioxidant enzymes; however, SelW deficiency did not affect the expression levels of antioxidants. These results suggest that SelW does not play a protective role against oxidative stress and insulin resistance in the skeletal muscle of high-fat diet-fed obese mice.

scholarly journals Myeloid-specific deletion of Zfp36 protects against insulin resistance and fatty liver in diet-induced obese mice

2018 ◽  
Vol 315 (4) ◽  
pp. E676-E693 ◽  
Author(s):  
Valentina Caracciolo ◽  
Jeanette Young ◽  
Donna Gonzales ◽  
Yingchun Ni ◽  
Stephen J. Flowers ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Mrna Expression ◽  
Zinc Finger Protein ◽  
Inflammatory Responses ◽  
Adipose Tissue Inflammation ◽  
Obese Mice ◽  
Tissue Inflammation ◽  
Mrna Binding

Obesity is associated with adipose tissue inflammation that contributes to insulin resistance. Zinc finger protein 36 (Zfp36) is an mRNA-binding protein that reduces inflammation by binding to cytokine transcripts and promoting their degradation. We hypothesized that myeloid-specific deficiency of Zfp36 would lead to increased adipose tissue inflammation and reduced insulin sensitivity in diet-induced obese mice. As expected, wild-type (Control) mice became obese and diabetic on a high-fat diet, and obese mice with myeloid-specific loss of Zfp36 [knockout (KO)] demonstrated increased adipose tissue and liver cytokine mRNA expression compared with Control mice. Unexpectedly, in glucose tolerance testing and hyperinsulinemic-euglycemic clamp studies, myeloid Zfp36 KO mice demonstrated improved insulin sensitivity compared with Control mice. Obese KO and Control mice had similar macrophage infiltration of the adipose depots and similar peripheral cytokine levels, but lean and obese KO mice demonstrated increased Kupffer cell (KC; the hepatic macrophage)-expressed Mac2 compared with lean Control mice. Insulin resistance in obese Control mice was associated with enhanced Zfp36 expression in KCs. Compared with Control mice, KO mice demonstrated increased hepatic mRNA expression of a multitude of classical (M1) inflammatory cytokines/chemokines, and this M1-inflammatory hepatic milieu was associated with enhanced nuclear localization of IKKβ and the p65 subunit of NF-κB. Our data confirm the important role of innate immune cells in regulating hepatic insulin sensitivity and lipid metabolism, challenge-prevailing models in which M1 inflammatory responses predict insulin resistance, and indicate that myeloid-expressed Zfp36 modulates the response to insulin in mice.

scholarly journals Double-Stranded RNA-Activated Protein Kinase Is a Key Modulator of Insulin Sensitivity in Physiological Conditions and in Obesity in Mice

Endocrinology ◽  
2012 ◽  
Vol 153 (11) ◽  
pp. 5261-5274 ◽  
Author(s):  
M. A. Carvalho-Filho ◽  
B. M. Carvalho ◽  
A. G. Oliveira ◽  
D. Guadagnini ◽  
M. Ueno ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Protein Phosphatase ◽  
High Fat Diet ◽  
Obese Mice ◽  
High Fat ◽  
Double Stranded Rna ◽  
Physiological Conditions ◽  
Phosphatase 2A

Abstract The molecular integration of nutrient- and pathogen-sensing pathways has become of great interest in understanding the mechanisms of insulin resistance in obesity. The double-stranded RNA-dependent protein kinase (PKR) is one candidate molecule that may provide cross talk between inflammatory and metabolic signaling. The present study was performed to determine, first, the role of PKR in modulating insulin action and glucose metabolism in physiological situations, and second, the role of PKR in insulin resistance in obese mice. We used Pkr−/− and Pkr+/+ mice to investigate the role of PKR in modulating insulin sensitivity, glucose metabolism, and insulin signaling in liver, muscle, and adipose tissue in response to a high-fat diet. Our data show that in lean Pkr−/− mice, there is an improvement in insulin sensitivity, and in glucose tolerance, and a reduction in fasting blood glucose, probably related to a decrease in protein phosphatase 2A activity and a parallel increase in insulin-induced thymoma viral oncogene-1 (Akt) phosphorylation. PKR is activated in tissues of obese mice and can induce insulin resistance by directly binding to and inducing insulin receptor substrate (IRS)-1 serine307 phosphorylation or indirectly through modulation of c-Jun N-terminal kinase and inhibitor of κB kinase β. Pkr−/− mice were protected from high-fat diet-induced insulin resistance and glucose intolerance and showed improved insulin signaling associated with a reduction in c-Jun N-terminal kinase and inhibitor of κB kinase β phosphorylation in insulin-sensitive tissues. PKR may have a role in insulin sensitivity under normal physiological conditions, probably by modulating protein phosphatase 2A activity and serine-threonine kinase phosphorylation, and certainly, this kinase may represent a central mechanism for the integration of pathogen response and innate immunity with insulin action and metabolic pathways that are critical in obesity.

scholarly journals Short-chain fatty acids: nutritional strategies to modulate intestinal microbiota

2021 ◽  
Vol 11 (5) ◽  
pp. 141-144
Author(s):  
Marcos Porto Arrais de Souza ◽  
Morgana Andrade Freitas ◽  
Carla Braga Campelo de Oliveira ◽  
Lorena Almeida Brito ◽  
Julio Cesar Chaves Nunes Filho ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Gastrointestinal Tract ◽  
Intestinal Microbiota ◽  
Short Chain Fatty Acids ◽  
Short Chain ◽  
Soluble Fiber ◽  
Fatty Acid Production ◽  
Pubmed Database ◽  
Nutritional Strategies ◽  
Chain Fatty Acids

Introduction: The intestinal microbiota has been the subject of research due to its association in physiological and pathological conditions. The production of short chain fatty acids obtained by fermentation of the intestinal microbiota has shown important effects on the gastrointestinal tract, adipose tissue, immune system and nervous system. Objective: This literature review aims to present different nutritional strategies with the potential to modulate the intestinal microbiota by increasing the production of short chain fatty acids. Methods: The research was considered a review work, through a bibliographic survey carried out from the collection of articles in English, published in the PubMed database, in the period from 2013 to 2020. The articles were selected from the descriptors: gut microbiota, soluble fiber, resistent starch, pectin, dietary fiber, short chain fatty acids (SCFA) with the combinations of the Boolean operators “and” and “or”. Studies considered as gray literature were excluded, as well as studies in which the titles were not related to the theme of the proposed research. Results: There are many benefits to consuming foods that may favor the increase of short chain fatty acids. This increase in the gastrointestinal tract is of fundamental importance for the maintenance of intestinal microbiota and prevention of diseases. Some nutritional strategies can be used in clinical therapy, such as increased consumption of fruits, vegetables and whole grains that are plant foods and important sources of fiber. The type of food must be observed, since each one can contain fibers of diverse types. Soluble fiber is the basis for the metabolization of short chain fatty acids and is found in various foods that can be inserted into the food plan, such as: bananas, apples, oats, barley, cooked and cooled potatoes, partially ground seeds, corn, morning cereal, agave, artichoke, asparagus, chicory root, garlic, onion, leeks and wheat. Conclusion: Scientific evidence of the relationship between nutrition, intestinal microbiota and short-chain fatty acid production demonstrates the importance of implementing simple nutritional strategies by health professionals, which can contribute to the modulation of the intestinal microbiota and the development of new perspectives in the development of therapies for prevention and treatment of diseases.

scholarly journals Evaluation of The Swelling Ability And Water Binding Capacity Of Some Local Plant Consumed In Adamawa State, Nigeria.

2020 ◽  
Vol 45 (5) ◽  
Author(s):  
N.M. Gaila ◽  
M. Buba ◽  
A. Ahmed
Keyword(s):  
Dietary Fiber ◽  
Functional Properties ◽  
Food Systems ◽  
Binding Capacity ◽  
Physicochemical Characteristics ◽  
Water Binding ◽  
Insoluble Dietary Fiber ◽  
Significant Difference ◽  
Local Plant ◽  
Water Swelling

The functional properties are the intrinsic physicochemical characteristics which affect the behavior of ingredient in food systems during processing, manufacturing, storage and preparation etc. Such functional properties include water and oil binding, emulsification capacities, swelling ability and viscosity. This work is aimed at evaluating the swelling Ability and water binding capacities of Spinous Amarantus (alayahon daji) (AA) Senna accedentalis (tasba) (TB), Phyllantus niruri (mace mai goyo) (MC), Hibiscus sabdrariffa (yakuwan daji) (YD) and Leptadenia hastate (yadiya) (YE) which are commonly consumed in our localities with little or no knowledge about their nutritional properties. AOAC method of analysis as outlined by Adabowale was adopted for the analysis with little modifications. All the samples analyzed showed significant water swelling ability with AA and YD showing the highest values of 1.5±0.06 v/g while TB shows the lowest value of 0.5±0.05 v/g. There was a significant difference (p <0.05) in the WBC values (%) obtained for the different plants analyzed. The results revealed that crude AA has the highest value of 12.48±0.82 and YD has the lowest value of 5.50±0.09. Insoluble dietary fiber (IDF) was also extracted from the samples and evaluated for water binding capacity. The Insoluble dietary fibre (IDF) showed WBC values. The highest values 1.54±0.08g/g and lowest 0.94±0.00g/g were obtained MC and YE respectively. All the crude samples showed significant water binding capacity (WBC) than their respective insoluble dietary fiber (IDF). This is as a result of the structural and chemical composition of the crude samples. However, the research has revealed that both the crude and the IDF samples analyzed has therapeutic potentials.

scholarly journals Digestive and metabolic effects of potato and maize fibres in human subjects

1997 ◽  
Vol 77 (1) ◽  
pp. 33-46 ◽  
Author(s):  
C. Cherbut ◽  
A.-C. Aube ◽  
N. Mekki ◽  
C. Dubois ◽  
D. Lairon ◽  
...  
Keyword(s):  
Transit Time ◽  
Binding Capacity ◽  
Human Subjects ◽  
Chemical Properties ◽  
Basal Diet ◽  
Metabolic Effects ◽  
Healthy Human ◽  
Water Binding ◽  
Blood Concentrations

The physiological effects of dietary fibres in humans are due to their physico-chemical properties. However, it is difficult to predict these effects simply by measuring certain characteristicsin vitro. Studies in human subjects are still required to assess the effectiveness of new substrates. The aim of the present study in healthy human subjects was to evaluate the effects of two novel fibres, potato (PF) and maize (MF), on fasting and postprandial blood concentrations of carbohydrate and lipid metabolites as well as on stool ouput and transit time. The chemical composition, water-binding capacity (WBC) and fermentative properties of the fibres were also characterized in order to determine their possible involvement in digestive and metabolic effects. Stools, as well as breath and blood samples, were collected after consumption for 1 month of either a basal diet (control) or a basal diet supplemented with fibre (15 g/d). MF resisted fermentation better than PF and had lower digestibility. However, both fibres increased faecal output of dry matter, neutral sugars and water. There was an inverse relationship between stool weight and orofaecal transit time, although only MF significantly reduced transit time. Orocaecal transit was lengthened by PF, probably because of its high WBC. PF ingestion also decreased postprandial plasma levels of total and esterified cholesterol but had no effect on fasting concentrations. In contrast, MF lowered fasting cholesterolaemia and increased free:esterified cholesterol. These particular physiological and fermentative properties suggest that PF and MF would be suitable ingredients in a healthy diet.

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