scholarly journals Sex Dependent Dysregulation of Hepatic Glucose Production in Lean Type 2 Diabetic Rats

2019 ◽  
Vol 10 ◽  
Author(s):  
Chellakkan S. Blesson ◽  
Amy Schutt ◽  
Shaji Chacko ◽  
Juan C. Marini ◽  
Pretty Rose Mathew ◽  
...  
Keyword(s):  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Diabetic Rats ◽  
Hepatic Glucose ◽  
Type 2 Diabetic

Irisin inhibits hepatic gluconeogenesis and increases glycogen synthesis via the PI3K/Akt pathway in type 2 diabetic mice and hepatocytes

2015 ◽  
Vol 129 (10) ◽  
pp. 839-850 ◽  
Author(s):  
Tong-Yan Liu ◽  
Chang-Xiang Shi ◽  
Run Gao ◽  
Hai-Jian Sun ◽  
Xiao-Qing Xiong ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Therapeutic Strategy ◽  
Hepatic Glucose Production ◽  
Glycogen Synthesis ◽  
Glucose Production ◽  
Hepatic Glycogen ◽  
Hepatic Glucose ◽  
Effective Therapeutic Strategy ◽  
Type 2 Diabetic

This study provide evidence that irisin reduces hepatic glucose production and the blood glucose level, increases hepatic glycogen synthesis and improves insulin resistance in type 2 diabetes. Irisin may be regarded as an effective therapeutic strategy for type 2 diabetes.

Glucagon dose-response curve for hepatic glucose production and glucose disposal in type 2 diabetic patients and normal individuals

Metabolism ◽  
2002 ◽  
Vol 51 (9) ◽  
pp. 1111-1119 ◽  
Author(s):  
Masafumi Matsuda ◽  
Ralph A. DeFronzo ◽  
Leonard Glass ◽  
Agostino Consoli ◽  
Mauro Giordano ◽  
...  
Keyword(s):  
Response Curve ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Glucose Disposal ◽  
Diabetic Patients ◽  
Type 2 Diabetic Patients ◽  
Normal Individuals ◽  
Hepatic Glucose ◽  
Type 2 Diabetic

scholarly journals Tiliacora triandra (Colebr.) Diels Leaf Aqueous Extract Inhibits Hepatic Glucose Production in HepG2 Cells and Type 2 Diabetic Rats

Molecules ◽  
2021 ◽  
Vol 26 (5) ◽  
pp. 1239
Author(s):  
Tipthida Pasachan ◽  
Acharaporn Duangjai ◽  
Atcharaporn Ontawong ◽  
Doungporn Amornlerdpison ◽  
Metee Jinakote ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Protein Kinase ◽  
Aqueous Extract ◽  
Hepg2 Cells ◽  
Antioxidant Activities ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Hepatic Glucose ◽  
Type 2 Diabetic

This study investigated the effects of Tiliacora triandra (Colebr.) Diels aqueous extract (TTE) on hepatic glucose production in hepatocellular carcinoma (HepG2) cells and type 2 diabetic (T2DM) conditions. HepG2 cells were pretreated with TTE and its major constituents found in TTE, epicatechin (EC) and quercetin (QC). The hepatic glucose production was determined. The in vitro data were confirmed in T2DM rats, which were supplemented daily with 1000 mg/kg body weight (BW) TTE, 30 mg/kg BW metformin or TTE combined with metformin for 12 weeks. Results demonstrate that TTE induced copper-zinc superoxide dismutase, glutathione peroxidase and catalase genes, similarly to EC and QC. TTE decreased hepatic glucose production by downregulating phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase) and increasing protein kinase B and AMP-activated protein kinase phosphorylation in HepG2 cells. These results correlated with the antihyperglycemic, antitriglyceridemic, anti-insulin resistance, and antioxidant activities of TTE in T2DM rats, similar to the metformin and combination treatments. Consistently, impairment of hepatic gluconeogenesis in T2DM rats was restored after single and combined treatments by reducing PEPCK and G6Pase genes. Collectively, TTE could potentially be developed as a nutraceutical product to prevent glucose overproduction in patients with obesity, insulin resistance, and diabetes who are being treated with antidiabetic drugs.

64-LB: Aerobic Exercise Decreases Hepatic Glucose Production via Asprosin Pathway in Diabetic Rats

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 64-LB
Author(s):  
JEONGRIM KO ◽  
TAE NYUN KIM ◽  
DAE YUN SEO ◽  
JIN HAN
Keyword(s):  
Aerobic Exercise ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Diabetic Rats ◽  
Hepatic Glucose

scholarly journals P0950EFFECT OF THYROID HORMONE TREATMENT ON RENAL REABSORPTION OF GLUCOSE IN ALLOXAN-INDUCED DIABETIC RATS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Gireesh Dayma
Keyword(s):  
Blood Glucose ◽  
Thyroid Hormone ◽  
Glucose Homeostasis ◽  
Hepatic Glucose Production ◽  
Liver Perfusion ◽  
Glucose Production ◽  
Diabetic Rats ◽  
Hepatic Glucose ◽  
Glucose Output ◽  
Renal Expression

Abstract Background and Aims The thyroid hormone (TH) plays an important role in glucose metabolism. Recently, we showed that the TH improves glycemia control by decreasing cytokines expression in the adipose tissue and skeletal muscle of alloxan-induced diabetic rats, which were also shown to present primary hypothyroidism. In this context, this study aims to investigate whether the chronic treatment of diabetic rats with T3 could affect other tissues that are involved in the control of glucose homeostasis, as the liver and kidney. Method Adult male Wistar rats were divided into nondiabetic, diabetic, and diabetic treated with T3 (1.5 ?g/100 g BW for 4 weeks). Diabetes was induced by alloxan monohydrate (150 mg/kg, BW, i.p.). Animals showing fasting blood glucose levels greater than 250 mg/dL were selected for the study. Results After treatment, we measured the blood glucose, serum T3, T4, TSH, and insulin concentration, hepatic glucose production by liver perfusion, liver PEPCK, GAPDH, and pAKT expression, as well as urine glucose concentration and renal expression of SGLT2 and GLUT2. T3 reduced blood glucose, hepatic glucose production, liver PEPCK, GAPDH, and pAKT content and the renal expression of SGLT2 and increased glycosuria. Conclusion Results suggest that the decreased hepatic glucose output and increased glucose excretion induced by T3 treatment are important mechanisms that contribute to reduce serum concentration of glucose, accounting for the improvement of glucose homeostasis control in diabetic rats.

scholarly journals Novel liver-specific TORC2 siRNA corrects hyperglycemia in rodent models of type 2 diabetes

2009 ◽  
Vol 297 (5) ◽  
pp. E1137-E1146 ◽  
Author(s):  
Maziyar Saberi ◽  
David Bjelica ◽  
Simon Schenk ◽  
Takeshi Imamura ◽  
Gautam Bandyopadhyay ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Primary Mouse Hepatocytes ◽  
Primary Mouse ◽  
Hepatic Glucose ◽  
Zdf Rats ◽  
Mouse Hepatocytes

The transcription factor TORC2 [transducer of regulated cAMP-responsive element-binding protein (CREB) activity 2] is a major regulator of hepatic gluconeogenesis and is increased in hyperglycemic rodent models. Because chronic hyperglycemia and increased hepatic glucose production, via increased gluconeogenesis, is a key feature of type 2 diabetes, an effective in vivo method to efficiently knock down TORC2 could provide a potential therapy for treating hyperglycemia and type 2 diabetes. To assess this, primary mouse hepatocytes, high-fat diet (HFD)-fed mice, and Zucker diabetic fatty (ZDF) rats were treated with a siRNA against TORC2 (siTORC2), which was delivered via a novel lipid nanoparticle system, or control siRNA (siCON). Compared with siCON, administration of siTORC2 resulted in highly efficient, sustained (1–3 wk) knockdown of TORC2 and its gluconeogenic target genes phospho enolpyruvate carboxykinase and glucose-6-phophatase in primary mouse hepatocytes and in the livers of HFD-fed mice. In mice, this knockdown was specific to the liver and did not occur in kidney, skeletal muscle, or adipose tissue. In HFD-fed mice, siTORC2 reduced in vivo gluconeogenic capacity, fasting hepatic glucose production, and hyperglycemia, and led to improved hepatic and skeletal muscle insulin sensitivity. siTORC2 treatment also improved systemic hyperglycemia in ZDF rats. In conclusion, these results demonstrate the importance of TORC2 in modulating HGP in vivo and highlight a novel, liver-specific siRNA approach for the potential treatment of hyperglycemia and type 2 diabetes.

scholarly journals Effect of 11β-hydroxysteroid dehydrogenase-1 inhibition on hepatic glucose metabolism in the conscious dog

2010 ◽  
Vol 298 (5) ◽  
pp. E1019-E1026 ◽  
Author(s):  
Dale S. Edgerton ◽  
Rita Basu ◽  
Christopher J. Ramnanan ◽  
Tiffany D. Farmer ◽  
Doss Neal ◽  
...  
Keyword(s):  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Hydroxysteroid Dehydrogenase ◽  
Insulin Deficiency ◽  
Potential Therapeutic Target ◽  
Hepatic Glucose Metabolism ◽  
Hepatic Glucose ◽  
Healthy Dogs ◽  
Excess Glucose

Inactive cortisone is converted to active cortisol within the liver by 11β-hydroxysteroid dehydrogenase-1 (11β-HSD1), and impaired regulation of this process may be related to increased hepatic glucose production (HGP) in individuals with type 2 diabetes. The primary aim of this study was to investigate the effect of acute 11β-HSD1 inhibition on HGP and fat metabolism during insulin deficiency. Sixteen conscious, 42-h-fasted, lean, healthy dogs were studied. Somatostatin was infused to create insulin deficiency, and the animals were treated with a specific 11β-HSD1 inhibitor (compound 531) or placebo for 5 h. 11β-HSD1 inhibition completely suppressed hepatic cortisol production, and this attenuated the increase in HGP that occurred during insulin deficiency. PEPCK and glucose-6-phosphatase expression were decreased when 11β-HSD1 was inhibited, but gluconeogenic flux was unchanged, implying an effect on glycogenolysis. Since inhibition of hepatic cortisol production reduces HGP during insulin deficiency, 11β-HSD1 is a potential therapeutic target for the treatment of excess glucose production that occurs in diabetes.

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