scholarly journals PA and OA Induce Abnormal Glucose Metabolism by Inhibiting KLF15 in Adipocytes

2021 ◽  
Author(s):  
Cuizhe Wang ◽  
Xiaolong Chu ◽  
Yuchun Deng ◽  
Jingzhou Wang ◽  
Tongtong Qiu ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
P38 Mapk ◽  
High Fat Diet ◽  
Elevated Serum ◽  
Glucose Levels ◽  
Abnormal Glucose Metabolism ◽  
Blood Glucose Levels ◽  
Visceral Adipose ◽  
Mapk Signal Pathway

Abstract Background: Obesity-induced elevated serum free fatty acids (FFAs) levels result in the occurrence of type 2 diabetes mellitus (T2DM). However, the molecular mechanism remains largely enigmatic. This study was to explore the effect and mechanism of KLF15 on FFAs-induced abnormal glucose metabolism. Methods: Levels of TG, TC, HDL-C, LDL-C, and glucose were measured by different assay kits. qRT-PCR and Western Blot were used to detect the levels of GPR120, GPR40, phosphorylation of p38 MAPK, KLF15, and downstream factors. Results: KLF15 was decreased in visceral adipose tissue of obesity subjects and high-fat diet (HFD) mice. In HFD mice, GPR120 antagonist significantly promoted KLF15 protein expression level and phosphorylation of p38 MAPK, meanwhile reduced the blood glucose levels. While, blocking GPR40 inhibited the KLF15 expression. In 3T3-L1 adipocytes, 1500 μM PA inhibited KLF15 through a GPR120/P-p38 MAPK signal pathway, and 750 μM OA inhibited KLF15 mainly through GPR120 while not dependent on P-p38 MAPK, ultimately resulting in abnormal glucose metabolism. Unfortunately, GPR40 didn’t contribute to PA or OA-induced KLF15 reduction. Conclusions: Both PA and OA inhibit KLF15 expression through GPR120, leading to abnormal glucose metabolism in adipocytes. Notably, the inhibition of KLF15 expression by PA depends on phosphorylation of p38 MAPK.

scholarly journals PA and OA induce abnormal glucose metabolism by inhibiting KLF15 in adipocytes

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Cuizhe Wang ◽  
Xiaolong Chu ◽  
Yuchun Deng ◽  
Jingzhou Wang ◽  
Tongtong Qiu ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
P38 Mapk ◽  
High Fat Diet ◽  
Elevated Serum ◽  
Glucose Levels ◽  
Abnormal Glucose Metabolism ◽  
Blood Glucose Levels ◽  
Visceral Adipose ◽  
Mapk Signal Pathway

Abstract Background Obesity-induced elevated serum free fatty acids (FFAs) levels result in the occurrence of type 2 diabetes mellitus (T2DM). However, the molecular mechanism remains largely enigmatic. This study was to explore the effect and mechanism of KLF15 on FFAs-induced abnormal glucose metabolism. Methods Levels of TG, TC, HDL-C, LDL-C, and glucose were measured by different assay kits. qRT-PCR and Western Blot were used to detect the levels of GPR120, GPR40, phosphorylation of p38 MAPK, KLF15, and downstream factors. Results KLF15 was decreased in visceral adipose tissue of obesity subjects and high-fat diet (HFD) mice. In HFD mice, GPR120 antagonist significantly promoted KLF15 protein expression level and phosphorylation of p38 MAPK, meanwhile reduced the blood glucose levels. While, blocking GPR40 inhibited the KLF15 expression. In 3T3-L1 adipocytes, 1500 μM PA inhibited KLF15 through a GPR120/P-p38 MAPK signal pathway, and 750 μM OA inhibited KLF15 mainly through GPR120 while not dependent on P-p38 MAPK, ultimately resulting in abnormal glucose metabolism. Unfortunately, GPR40 didn’t contribute to PA or OA-induced KLF15 reduction. Conclusions Both PA and OA inhibit KLF15 expression through GPR120, leading to abnormal glucose metabolism in adipocytes. Notably, the inhibition of KLF15 expression by PA depends on phosphorylation of p38 MAPK.

scholarly journals Nighttime Administration of Nicotine Improves Hepatic Glucose Metabolism via the Hypothalamic Orexin System in Mice

Endocrinology ◽  
2016 ◽  
Vol 157 (1) ◽  
pp. 195-206 ◽  
Author(s):  
Hiroshi Tsuneki ◽  
Takashi Nagata ◽  
Mikio Fujita ◽  
Kanta Kon ◽  
Naizhen Wu ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Glucose Metabolism ◽  
Oral Intake ◽  
Mrna Levels ◽  
Active Period ◽  
Wild Type ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Deficient Mice

Abstract Nicotine is known to affect the metabolism of glucose; however, the underlying mechanism remains unclear. Therefore, we here investigated whether nicotine promoted the central regulation of glucose metabolism, which is closely linked to the circadian system. The oral intake of nicotine in drinking water, which mainly occurred during the nighttime active period, enhanced daily hypothalamic prepro-orexin gene expression and reduced hyperglycemia in type 2 diabetic db/db mice without affecting body weight, body fat content, and serum levels of insulin. Nicotine administered at the active period appears to be responsible for the effect on blood glucose, because nighttime but not daytime injections of nicotine lowered blood glucose levels in db/db mice. The chronic oral treatment with nicotine suppressed the mRNA levels of glucose-6-phosphatase, the rate-limiting enzyme of gluconeogenesis, in the liver of db/db and wild-type control mice. In the pyruvate tolerance test to evaluate hepatic gluconeogenic activity, the oral nicotine treatment moderately suppressed glucose elevations in normal mice and mice lacking dopamine receptors, whereas this effect was abolished in orexin-deficient mice and hepatic parasympathectomized mice. Under high-fat diet conditions, the oral intake of nicotine lowered blood glucose levels at the daytime resting period in wild-type, but not orexin-deficient, mice. These results indicated that the chronic daily administration of nicotine suppressed hepatic gluconeogenesis via the hypothalamic orexin-parasympathetic nervous system. Thus, the results of the present study may provide an insight into novel chronotherapy for type 2 diabetes that targets the central cholinergic and orexinergic systems.

scholarly journals Prediabetes

JMS SKIMS ◽  
2011 ◽  
Vol 14 (1) ◽  
pp. 4-10
Author(s):  
Mir Iftikhar Bashir ◽  
Arshad Iqbal Wani ◽  
Shariq R Masoodi
Keyword(s):  
Diabetes Mellitus ◽  
Beta Cell Dysfunction ◽  
Expert Committee ◽  
Committee Report ◽  
Glucose Levels ◽  
Cell Dysfunction ◽  
Abnormal Glucose Metabolism ◽  
Blood Glucose Levels

Pre-diabetes is a metabolic condition characterized by insulin resistance and primary or secondary beta cell dysfunction which increases the risk of developing type 2 diabetes mellitus. It is used to describe the intermediate state of abnormal glucose metabolism in which blood glucose levels are higher than normal, but not yet in the range necessary for diagnosis of diabetes. The concept of prediabetes arose in 1950’s when high perinatal mortality was reported in pregnancies before diagnosis of diabetes mellitus. Prediabetes was included in the classification of glucose tolerance in the 1965 WHO Expert Committee Report on Diabetes Mellitus...JMS 2011;14(1):4-10.

scholarly journals Ishige okamurae reduces blood glucose levels in high-fat diet mice and improves glucose metabolism in the skeletal muscle and pancreas

2020 ◽  
Vol 23 (1) ◽  
Author(s):  
Hye-Won Yang ◽  
Myeongjoo Son ◽  
Junwon Choi ◽  
Seyeon Oh ◽  
You-Jin Jeon ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Glucose ◽  
Glucose Metabolism ◽  
Blood Glucose Level ◽  
High Fat Diet ◽  
Saline Group ◽  
High Fat ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Ishige Okamurae

Abstract Brown alga (Ishige okamurae; IO) dietary supplements have been reported to possess anti-diabetic properties. However, the effects of IO supplements have not been evaluated on glucose metabolism in the pancreas and skeletal muscle. C57BL/6 N male mice (age, 7 weeks) were arranged in five groups: a chow diet with 0.9% saline (NFD/saline group), high-fat diet (HFD) with 0.9% saline (HFD/saline group). high-fat diet with 25 mg/kg IO extract (HFD/25/IOE). high-fat diet with 50 mg/kg IO extract (HFD/50/IOE), and high-fat diet with 75 mg/kg IO extract (HFD/75/IOE). After 4 weeks, the plasma, pancreas, and skeletal muscle samples were collected for biochemical analyses. IOE significantly ameliorated glucose tolerance impairment and fasting and 2 h blood glucose level in HFD mice. IOE also stimulated the protein expressions of the glucose transporters (GLUTs) including GLUT2 and GLUT4 and those of their related transcription factors in the pancreases and skeletal muscles of HFD mice, enhanced glucose metabolism, and regulated blood glucose level. Our results suggest Ishige okamurae extract may reduce blood glucose levels by improving glucose metabolism in the pancreas and skeletal muscle in HFD-induced diabetes.

scholarly journals The influence of novel GPR119 agonist on body weight, food intake and glucose metabolism in obesity rats provoked high-fat and -carbohydrate diet

2016 ◽  
Vol 62 (1) ◽  
pp. 44-49 ◽  
Author(s):  
Ivan Nikolaevich Tiurenkov ◽  
Denis Vladimirovich Kurkin ◽  
Dmitry Aleksandrovich Bakulin ◽  
Elena Vladimirovna Volotova ◽  
Mikhail Ayratovich Chafeev
Keyword(s):  
Body Weight ◽  
Blood Glucose ◽  
Food Intake ◽  
Glucose Metabolism ◽  
High Fat Diet ◽  
High Fat ◽  
Glucose Levels ◽  
High Carbohydrate ◽  
Blood Glucose Levels ◽  
Gpr119 Agonist

The search for new drugs for the treatment of type 2 diabetes mellitus (T2DM) and obesity remains an urgent problem. Drugs with influence on incretin system are widely used in the treatment of T2DM and obesity, since in addition to the hypoglycemic action of their inherent hypophagic effects. With the discovery of GPR119 receptor, there is the opportunity to pharmacological stimulation of endogenous secretion of incretins. Compound ZB-16 is active GPR119 agonist with IC50=7 nM. Its activation leads to increased secretion of the major incretins (GLP-1 and GIP), which are able to influence glucose metabolism and feeding behavior.Aims — to study the effect of GPR 119 receptor agonist compounds ZB-16 on blood glucose, body weight and food intake in rats with obesity.Material and methods.Male rats with initial weight 390—400 g were fed with high-carbohydrate and high-fat diet. During the next four weeks the animals orally received ZB-16 (1 mg/kg) and metformin (400 mg/kg) and then we assessed the level of water and food consumption, blood glucose levels, and performed oral glucose tolerance test (OGTT).Results.Compound ZB-16 and metformin reduced fasting blood glucose levels and weight of experimental animals, while the control rats gained weight. GPR119 agonist is more pronounced than metformin reduced the area under the curve «glucose of concentration—time» during the OGTT.Conclusions.Novel GPR119 agonist — ZB-16 is comparable to metformin in hypoglycemic and anorexigenic effect in animals with obesity caused high-carbohydrate and high-fat diet.

scholarly journals Galectin-3 Deletion Enhances Visceral Adipose Tissue Inflammation and Dysregulates Glucose Metabolism in Mice on a High-Fat Diet

2016 ◽  
Vol 17 (3) ◽  
pp. 231-240 ◽  
Author(s):  
Ilija Jeftic ◽  
Marina Miletic-Kovacevic ◽  
Nemanja Jovicic ◽  
Jelena Pantic ◽  
Nebojsa Arsenijevic ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Glucose Metabolism ◽  
Visceral Adipose Tissue ◽  
High Fat Diet ◽  
High Fat ◽  
Galectin 3 ◽  
Visceral Adipose

Abstract Obesity and type 2 diabetes mellitus (T2DM) constitute major health problems worldwide. Increased visceral adiposity enhances the risk of insulin resistance and type 2 diabetes. The mechanisms involved in obesity-associated chronic inflammation in metabolic tissues (metaflammation) that lead to insulin resistance and dysregulated glucose metabolism are incompletely defined. Galectin-3 (Gal-3), a β-galactoside-binding lectin, modulates immune/inflammatory responses and specifically binds to metabolic danger molecules. To dissect the role of Gal-3 in obesity and diabetes, Gal-3-deficient (LGALS3-/-) and wild-type (WT) C57Bl/6 male mice were placed on a high-fat diet (HFD, 60% kcal fat) or a standard chow diet (10% kcal fat) for 6 months and metabolic, histological and immunophenotypical analyses of the visceral adipose tissue were performed. HFD-fed LGALS3-/- mice had higher body weights and more body weight gain, visceral adipose tissue (VAT), hyperglycaemia, hyperinsulinemia, insulin resistance and hyperlipidemia than diet-matched WT mice. Compared to WT mice, the enlarged VAT in obese LGALS3-/- mice contained larger adipocytes. Additionally, we demonstrate enhanced inflammation in the VAT of LGALS3-/- mice compared with diet-matched WT mice. The VAT of LGALS3-/- mice fed a HFD contained more numerous dendritic cells and proinflammatory F4/80+CD11c+CD11b+ and F4/80high macrophages. In contrast to WT mice, the numbers of CXCR3+ and CD8+ T cells were increased in the VAT of Gal-3-deficient mice after 6 months of high-fat feeding. We provide evidence that Gal-3 ablation results in enhanced HFD-induced adiposity, inflammation in the adipose tissue, insulin resistance and hyperglycaemia. Thus, Gal-3 represents an important regulator of obesity-associated immunometabolic alterations.

scholarly journals Glucose metabolism responds to perceived sugar intake more than actual sugar intake

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Chanmo Park ◽  
Francesco Pagnini ◽  
Ellen Langer
Keyword(s):  
Type 2 Diabetes ◽  
Blood Glucose ◽  
Glucose Metabolism ◽  
Diabetes Management ◽  
Psychological Intervention ◽  
Sugar Intake ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Study Results

Abstract The authors examine study participants who have Type 2 diabetes to determine whether cognition affects glucose levels in contrast to widely held suppositions. Thirty participants who have type 2 diabetes consume beverages that have identical ingredients but have deceptive nutrition facts labels. Blood glucose levels measured four times before and after beverage consumption show that blood glucose levels increase when participants believe the beverage has high sugar content as portrayed on the labels. Also, individual eating behaviors and nutritional satisfaction are linked to changes in blood glucose levels. The study results support the concept of anticipatory budgeting on glucose metabolism. The findings provide pressing evidence for the psychobiological model of chronic disease, suggesting that psychological intervention programs may be important for diabetes management, beyond current programs in which type 2 diabetes is managed through diet, exercise, and medications only.

scholarly journals Fermented Rice Germ Extract Ameliorates Abnormal Glucose Metabolism via Antioxidant Activity in Type 2 Diabetes Mellitus Mice

2021 ◽  
Vol 11 (7) ◽  
pp. 3091
Author(s):  
Ye Ji Hyun ◽  
Ju Gyeong Kim ◽  
Sung Keun Jung ◽  
Ji Yeon Kim
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Metabolism ◽  
Ferulic Acid ◽  
Fasting Blood Glucose ◽  
Liver Weight ◽  
Glucose Levels ◽  
Hepatic Glucose Metabolism ◽  
Abnormal Glucose Metabolism ◽  
Hepatic Glucose

Rice germ is an abundant source of ferulic acid, which is known for its anti-oxidant activity. This study aimed to evaluate the regulatory effects of fermented rice germ extracts on hepatic glucose metabolism in C57BL/KsJ-db/db mice. Rice germ was fermented with Lactobacillus plantarum and extracted with 30% ethanol (RG_30E) or 50% ethanol (RG_50E). Mice were fed modified AIN-93 diets containing fermented rice germ extracts and ferulic acid for 8 weeks. RG_50E significantly reduced food intake as well as liver weight and RG_30E and RG_50E improved glucose homeostasis, as indicated by fasting blood glucose levels and glucose tolerance. Hepatic triglyceride and total cholesterol levels were significantly decreased in db/db mice fed RG_30E and RG_50E. The antioxidant capacity of RG_30E and RG_50E was confirmed by a decrease in malondialdehyde levels and an increase in hepatic superoxide dismutase activity. The expression of genes related to glycolysis and gluconeogenesis was significantly regulated by RG_30E and RG_50E. These results suggest that fermented rice germ extracts have the potential to regulate hypoglycemia and hepatic glucose metabolism in type 2 diabetes db/db mice.

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