scholarly journals In vivo multi-tissue efficacy of peroxisome proliferator-activated receptor-γ therapy on glucose and fatty acid metabolism in obese type 2 diabetic rats

Obesity ◽  
2013 ◽  
Vol 21 (12) ◽  
pp. 2522-2529 ◽  
Author(s):  
Samuel Nemanich ◽  
Sudheer Rani ◽  
Kooresh Shoghi
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Diabetic Rats ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Type 2 Diabetic

scholarly journals Genomic and Metabolic Disposition of Non-Obese Type 2 Diabetic Rats to Increased Myocardial Fatty Acid Metabolism

PLoS ONE ◽  
2013 ◽  
Vol 8 (10) ◽  
pp. e78477 ◽  
Author(s):  
Sriram Devanathan ◽  
Samuel T. Nemanich ◽  
Attila Kovacs ◽  
Nicole Fettig ◽  
Robert J. Gropler ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Diabetic Rats ◽  
Myocardial Fatty Acid ◽  
Myocardial Fatty Acid Metabolism ◽  
Type 2 Diabetic ◽  
Metabolic Disposition

scholarly journals Anti-influenza A Virus Effects and Mechanisms of Emodin and Its Analogs via Regulating PPARα/γ-AMPK-SIRT1 Pathway and Fatty Acid Metabolism

2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Yufei Bei ◽  
Boyu Tia ◽  
Yuze Li ◽  
Yingzhu Guo ◽  
Shufei Deng ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Influenza A Virus ◽  
Fatty Acid Metabolism ◽  
Influenza A ◽  
Acid Metabolism ◽  
Fatty Acid Biosynthesis ◽  
Sirtuin 1 ◽  
Peroxisome Proliferator ◽  
In Vivo Test

The peroxisome proliferator-activated receptor (PPAR) α/γ-adenosine 5 ′ -monophosphate- (AMP-) activated protein kinase- (AMPK-) sirtuin-1 (SIRT1) pathway and fatty acid metabolism are reported to be involved in influenza A virus (IAV) replication and IAV-pneumonia. Through a cell-based peroxisome proliferator responsive element- (PPRE-) driven luciferase bioassay, we have investigated 145 examples of traditional Chinese medicines (TCMs). Several TCMs, such as Polygonum cuspidatum, Rheum officinale Baillon, and Aloe vera var. Chinensis (Haw.) Berg., were found to possess high activity. We have further detected the anti-IAV activities of emodin (EMO) and its analogs, a group of common important compounds of these TCMs. The results showed that emodin and its several analogs possess excellent anti-IAV activities. The pharmacological tests showed that emodin significantly activated PPARα/γ and AMPK, decreased fatty acid biosynthesis, and increased intracellular ATP levels. Pharmaceutical inhibitors, siRNAs for PPARα/γ and AMPKα1, and exogenous palmitate impaired the inhibition of emodin. The in vivo test also showed that emodin significantly protected mice from IAV infection and pneumonia. Pharmacological inhibitors for PPARα/γ and AMPK signal and exogenous palmitate could partially counteract the effects of emodin in vivo. In conclusion, emodin and its analogs are a group of promising anti-IAV drug precursors, and the pharmacological mechanism of emodin is linked to its ability to regulate the PPARα/γ-AMPK pathway and fatty acid metabolism.

Impaired fatty acid metabolism in type 2 diabetic skeletal muscle cells is reversed by PPARγ agonists

2005 ◽  
Vol 289 (1) ◽  
pp. E151-E159 ◽  
Author(s):  
Bong-Soo Cha ◽  
Theodore P. Ciaraldi ◽  
Kyong-Soo Park ◽  
Leslie Carter ◽  
Sunder R. Mudaliar ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Muscle Cells ◽  
Palmitate Oxidation ◽  
Pparγ Agonists ◽  
Type 2 Diabetic

The impact of type 2 diabetes on the ability of muscle to accumulate and dispose of fatty acids and triglycerides was evaluated in cultured muscle cells from nondiabetic (ND) and type 2 diabetic (T2D) subjects. In the presence of 5 μM palmitate, T2D muscle cells accumulated less lipid than ND cells (11.5 ± 1.2 vs. 15.1 ± 1.4 nmol/mg protein, P < 0.05). Chronic treatment (4 days) with the peroxisome proliferator-activated receptor-γ (PPARγ) agonist troglitazone increased palmitate accumulation, normalizing uptake in T2D cells. There were no significant differences between groups with regard to the relative incorporation of palmitate into neutral lipid species. This distribution was also unaffected by troglitazone treatment. β-Oxidation of both long-chain (palmitate) and medium-chain (octanoate) fatty acids in T2D muscle cells was reduced by ∼40% compared with ND cells. Palmitate oxidation occurred primarily in mitochondrial (∼40–50% of total) and peroxisomal (20–30%) compartments. The diabetes-related defect in palmitate oxidation was localized to the mitochondrial component. Both palmitate and octanoate oxidation were stimulated by a series of thiazolidinediones. Oxidation in T2D muscle cells was normalized after treatment. Troglitazone increased the mitochondrial component of palmitate oxidation. Skeletal muscle cells from T2D subjects express defects in free fatty acid metabolism that are retained in vitro, most importantly defects in β-oxidation. These defects can be corrected by treatment with PPARγ agonists. Augmentation of fatty acid disposal in skeletal muscle, potentially reducing intramyocellular triglyceride content, may represent one mechanism for the lipid-lowering and insulin-sensitizing effects of thiazolidinediones.

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