Supplementation of Chitosan Alleviates High-Fat Diet-Enhanced Lipogenesis in Rats via Adenosine Monophosphate (AMP)-Activated Protein Kinase Activation and Inhibition of Lipogenesis-Associated Genes

2015 ◽  
Vol 63 (11) ◽  
pp. 2979-2988 ◽  
Author(s):  
Chen-Yuan Chiu ◽  
Im-Lam Chan ◽  
Tsung-Han Yang ◽  
Shing-Hwa Liu ◽  
Meng-Tsan Chiang
Keyword(s):  
Protein Kinase ◽  
High Fat Diet ◽  
Adenosine Monophosphate ◽  
High Fat ◽  
Kinase Activation ◽  
Protein Kinase Activation ◽  
Amp Activated Protein Kinase

scholarly journals AMP-activated protein kinase activation ameliorates eicosanoid dysregulation in high-fat-induced kidney disease in mice

2019 ◽  
Vol 60 (5) ◽  
pp. 937-952 ◽  
Author(s):  
Anne-Emilie Declèves ◽  
Anna V. Mathew ◽  
Aaron M. Armando ◽  
Xianlin Han ◽  
Edward A. Dennis ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Kidney Disease ◽  
Ampk Activation ◽  
High Fat ◽  
Kinase Activation ◽  
Venous Circulation ◽  
Protein Kinase Activation ◽  
Anti Inflammatory ◽  
Amp Activated Protein Kinase

High-fat diet (HFD) causes renal lipotoxicity that is ameliorated with AMP-activated protein kinase (AMPK) activation. Although bioactive eicosanoids increase with HFD and are essential in regulation of renal disease, their role in the inflammatory response to HFD-induced kidney disease and their modulation by AMPK activation remain unexplored. In a mouse model, we explored the effects of HFD on eicosanoid synthesis and the role of AMPK activation in ameliorating these changes. We used targeted lipidomic profiling with quantitative MS to determine PUFA and eicosanoid content in kidneys, urine, and renal arterial and venous circulation. HFD increased phospholipase expression as well as the total and free pro-inflammatory arachidonic acid (AA) and anti-inflammatory DHA in kidneys. Consistent with the parent PUFA levels, the AA- and DHA-derived lipoxygenase (LOX), cytochrome P450, and nonenzymatic degradation (NE) metabolites increased in kidneys with HFD, while EPA-derived LOX and NE metabolites decreased. Conversely, treatment with 5-aminoimidazole-4-carboxamide-1-β-D-furanosyl 5′-monophosphate (AICAR), an AMPK activator, reduced the free AA and DHA content and the DHA-derived metabolites in kidney. Interestingly, kidney and circulating AA, AA metabolites, EPA-derived LOX, and NE metabolites are increased with HFD; whereas, DHA metabolites are increased in kidney in contrast to their decreased circulating levels with HFD. Together, these changes showcase HFD-induced pro- and anti-inflammatory eicosanoid dysregulation and highlight the role of AMPK in correcting HFD-induced dysregulated eicosanoid pathways.

scholarly journals Loss of CTRP1 disrupts glucose and lipid homeostasis

2016 ◽  
Vol 311 (4) ◽  
pp. E678-E697 ◽  
Author(s):  
Susana Rodriguez ◽  
Xia Lei ◽  
Pia S. Petersen ◽  
Stefanie Y. Tan ◽  
Hannah C. Little ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
High Fat Diet ◽  
Glucose Transporter ◽  
Lipid Synthesis ◽  
High Fat ◽  
Kinase Activation ◽  
Cholesterol Levels ◽  
Protein Kinase Activation ◽  
Amp Activated Protein Kinase

C1q/TNF-related protein 1 (CTRP1) is a conserved plasma protein of the C1q family with notable metabolic and cardiovascular functions. We have previously shown that CTRP1 infusion lowers blood glucose and that transgenic mice with elevated circulating CTRP1 are protected from diet-induced obesity and insulin resistance. Here, we used a genetic loss-of-function mouse model to address the requirement of CTRP1 for metabolic homeostasis. Despite similar body weight, food intake, and energy expenditure, Ctrp1 knockout (KO) mice fed a low-fat diet developed insulin resistance and hepatic steatosis. Impaired glucose metabolism in Ctrp1 KO mice was associated with increased hepatic gluconeogenic gene expression and decreased skeletal muscle glucose transporter glucose transporter 4 levels and AMP-activated protein kinase activation. Loss of CTRP1 enhanced the clearance of orally administered lipids but did not affect intestinal lipid absorption, hepatic VLDL-triglyceride export, or lipoprotein lipase activity. In contrast to triglycerides, hepatic cholesterol levels were reduced in Ctrp1 KO mice, paralleling the reduced expression of cholesterol synthesis genes. Contrary to expectations, when challenged with a high-fat diet to induce obesity, Ctrp1 KO mice had increased physical activity and reduced body weight, adiposity, and expression of lipid synthesis and fibrotic genes in adipose tissue; these phenotypes were linked to elevated FGF-21 levels. Due in part to increased hepatic AMP-activated protein kinase activation and reduced expression of lipid synthesis genes, Ctrp1 KO mice fed a high-fat diet also had reduced liver and serum triglyceride and cholesterol levels. Taken together, these results provide genetic evidence to establish the significance of CTRP1 to systemic energy metabolism in different metabolic and dietary contexts.

scholarly journals Insulin antagonizes AMP-activated protein kinase activation by ischemia or anoxia in rat hearts, without affecting total adenine nucleotides

FEBS Letters ◽  
2001 ◽  
Vol 505 (3) ◽  
pp. 348-352 ◽  
Author(s):  
Christophe Beauloye ◽  
Anne-Sophie Marsin ◽  
Luc Bertrand ◽  
Ulrike Krause ◽  
D.Grahame Hardie ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Adenine Nucleotides ◽  
Kinase Activation ◽  
Protein Kinase Activation ◽  
Rat Hearts ◽  
Amp Activated Protein Kinase

scholarly journals Beneficial Role of Erythrocyte Adenosine A2B Receptor–Mediated AMP-Activated Protein Kinase Activation in High-Altitude Hypoxia

Circulation ◽  
2016 ◽  
Vol 134 (5) ◽  
pp. 405-421 ◽  
Author(s):  
Hong Liu ◽  
Yujin Zhang ◽  
Hongyu Wu ◽  
Angelo D’Alessandro ◽  
Gennady G. Yegutkin ◽  
...  
Keyword(s):  
Protein Kinase ◽  
High Altitude ◽  
Altitude Hypoxia ◽  
Kinase Activation ◽  
Beneficial Role ◽  
Protein Kinase Activation ◽  
A2b Receptor ◽  
Amp Activated Protein Kinase ◽  
Adenosine A2b
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