scholarly journals Ginsenoside Rg1 Suppresses Hepatic Glucose Production via AMP-Activated Protein Kinase in HepG2 Cells

2010 ◽  
Vol 33 (2) ◽  
pp. 325-328 ◽  
Author(s):  
Sung Jip Kim ◽  
Hai Dan Yuan ◽  
Sung Hyun Chung
Keyword(s):  
Protein Kinase ◽  
Hepg2 Cells ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Ginsenoside Rg1 ◽  
Hepatic Glucose ◽  
Amp Activated Protein Kinase

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.

Regulation of Hepatic Glucose Production by Transforming Growth Factor Beta 1 via Protein Kinase A

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 2441-PUB ◽  
Author(s):  
QUAN PAN ◽  
YUNMEI CHEN ◽  
HUI YAN ◽  
WANBAO YANG ◽  
ZHENG SHEN ◽  
...  
Keyword(s):  
Growth Factor ◽  
Protein Kinase ◽  
Protein Kinase A ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Hepatic Glucose ◽  
Growth Factor Beta ◽  
Kinase A

scholarly journals Geniposide Suppresses Hepatic Glucose Production via AMPK in HepG2 Cells

2016 ◽  
Vol 39 (4) ◽  
pp. 484-491 ◽  
Author(s):  
Lixia Guo ◽  
Xuxu Zheng ◽  
Jianhui Liu ◽  
Zhongyi Yin
Keyword(s):  
Hepg2 Cells ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Hepatic Glucose

scholarly journals mTOR Inhibitor Therapy and Metabolic Consequences: Where Do We Stand?

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Aleksandra Kezic ◽  
Ljiljana Popovic ◽  
Katarina Lalic
Keyword(s):  
Protein Kinase ◽  
Glucose Metabolism ◽  
Calorie Restriction ◽  
Mtor Inhibitor ◽  
Hepatic Glucose Production ◽  
Mtor Inhibitors ◽  
Glucose Production ◽  
Metabolic Effects ◽  
Solid Organ ◽  
Amp Activated Protein Kinase

mTOR (mechanistic target of rapamycin) protein kinase acts as a central integrator of nutrient signaling pathways. Besides the immunosuppressive role after solid organ transplantations or in the treatment of some cancers, another promising role of mTOR inhibitor as an antiaging therapeutic has emerged in the recent years. Acute or intermittent rapamycin treatment has some resemblance to calorie restriction in metabolic effects such as an increased insulin sensitivity. However, the chronic inhibition of mTOR by macrolide rapamycin or other rapalogs has been associated with glucose intolerance and insulin resistance and may even provoke type II diabetes. These metabolic adverse effects limit the use of mTOR inhibitors. Metformin is a widely used drug for the treatment of type 2 diabetes which activates AMP-activated protein kinase (AMPK), acting as calorie restriction mimetic. In addition to the glucose-lowering effect resulting from the decreased hepatic glucose production and increased glucose utilization, metformin induces fatty acid oxidations. Here, we review the recent advances in our understanding of the metabolic consequences regarding glucose metabolism induced by mTOR inhibitors and compare them to the metabolic profile provoked by metformin use. We further suggest metformin use concurrent with rapalogs in order to pharmacologically address the impaired glucose metabolism and prevent the development of new-onset diabetes mellitus after solid organ transplantations induced by the chronic rapalog treatment.

Olanzapine increases hepatic glucose production through the activation of hypothalamic adenosine 5′-monophosphate-activated protein kinase

2013 ◽  
Vol 15 (12) ◽  
pp. 1128-1135 ◽  
Author(s):  
M. Ikegami ◽  
H. Ikeda ◽  
T. Ohashi ◽  
M. Ohsawa ◽  
Y. Ishikawa ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Hepatic Glucose

Cis ‐9, Trans ‐11 Conjugated Linoleic Acid Reduces Phosphoenolpyruvate Carboxykinase Expression and Hepatic Glucose Production in HepG2 Cells

Lipids ◽  
2019 ◽  
Vol 54 (6-7) ◽  
pp. 369-379
Author(s):  
Boon Kheng Chai ◽  
Mustafa Al‐Shagga ◽  
Yan Pan ◽  
Sue‐Mian Then ◽  
Kang Nee Ting ◽  
...  
Keyword(s):  
Linoleic Acid ◽  
Conjugated Linoleic Acid ◽  
Hepg2 Cells ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Hepatic Glucose

FGF21 suppresses hepatic glucose production through the activation of atypical protein kinase Cι/λ

2013 ◽  
Vol 702 (1-3) ◽  
pp. 302-308 ◽  
Author(s):  
Ling-Jie Kong ◽  
Wen Feng ◽  
Michael Wright ◽  
Yuli Chen ◽  
Qing Dallas-yang ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Atypical Protein Kinase ◽  
Hepatic Glucose

scholarly journals Fructose-Induced Hypothalamic AMPK Activation Stimulates Hepatic PEPCK and Gluconeogenesis due to Increased Corticosterone Levels

Endocrinology ◽  
2012 ◽  
Vol 153 (8) ◽  
pp. 3633-3645 ◽  
Author(s):  
Andrezza Kinote ◽  
Juliana A. Faria ◽  
Erika A. Roman ◽  
Carina Solon ◽  
Daniela S. Razolli ◽  
...  
Keyword(s):  
Glucocorticoid Receptor ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Ampk Activation ◽  
Hepatic Gluconeogenesis ◽  
Compound C ◽  
Ampk Phosphorylation ◽  
Hepatic Glucose ◽  
Amp Activated Protein Kinase ◽  
Interfering Rna

Fructose consumption causes insulin resistance and favors hepatic gluconeogenesis through mechanisms that are not completely understood. Recent studies demonstrated that the activation of hypothalamic 5′-AMP-activated protein kinase (AMPK) controls dynamic fluctuations in hepatic glucose production. Thus, the present study was designed to investigate whether hypothalamic AMPK activation by fructose would mediate increased gluconeogenesis. Both ip and intracerebroventricular (icv) fructose treatment stimulated hypothalamic AMPK and acetyl-CoA carboxylase phosphorylation, in parallel with increased hepatic phosphoenolpyruvate carboxy kinase (PEPCK) and gluconeogenesis. An increase in AMPK phosphorylation by icv fructose was observed in the lateral hypothalamus as well as in the paraventricular nucleus and the arcuate nucleus. These effects were mimicked by icv 5-amino-imidazole-4-carboxamide-1-β-d-ribofuranoside treatment. Hypothalamic AMPK inhibition with icv injection of compound C or with injection of a small interfering RNA targeted to AMPKα2 in the mediobasal hypothalamus (MBH) suppressed the hepatic effects of ip fructose. We also found that fructose increased corticosterone levels through a mechanism that is dependent on hypothalamic AMPK activation. Concomitantly, fructose-stimulated gluconeogenesis, hepatic PEPCK expression, and glucocorticoid receptor binding to the PEPCK gene were suppressed by pharmacological glucocorticoid receptor blockage. Altogether the data presented herein support the hypothesis that fructose-induced hypothalamic AMPK activation stimulates hepatic gluconeogenesis by increasing corticosterone levels.

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