Tissue-specific actions of antidiabetic thiazolidinediones on the reduced fatty acid oxidation in skeletal muscle and liver of zucker diabetic fatty rats

Ide, Tomohiro; Nakazawa, Tomoko; Mochizuki, Toru; Murakami, Koji

doi:10.1016/s0026-0495(00)80019-0

Cited by 39 publications

(31 citation statements)

References 26 publications

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“…Directing FFA to the mitochondria for oxidation may prevent them (either in their free form or as triglycerides) from causing insulin resistance. Consistent with this postulate, thiazolidinediones have been found to increase uptake and oxidation of FFA by muscle in several animal models of insulin resistance (16,33). Other investigators have found a contrasting result, Tgz inhibition of palmitate oxidation in isolated soleus muscle (13).…”

Section: Discussionmentioning

confidence: 77%

Thiazolidinediones upregulate impaired fatty acid uptake in skeletal muscle of type 2 diabetic subjects

Wilmsen

Ciaraldi

Carter

et al. 2003

American Journal of Physiology-Endocrinology and Metabolism

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We examined the regulation of free fatty acid (FFA, palmitate) uptake into skeletal muscle cells of nondiabetic and type 2 diabetic subjects. Palmitate uptake included a protein-mediated component that was inhibited by phloretin. The protein-mediated component of uptake in muscle cells from type 2 diabetic subjects (78 ± 13 nmol · mg protein-1 · min-1) was reduced compared with that in nondiabetic muscle (150 ± 17, P < 0.01). Acute insulin exposure caused a modest (16 ± 5%, P < 0.025) but significant increase in protein-mediated uptake in nondiabetic muscle. There was no significant insulin effect in diabetic muscle (+19 ± 19%, P = not significant). Chronic (4 day) treatment with a series of thiazolidinediones, troglitazone (Tgz), rosiglitazone (Rgz), and pioglitazone (Pio) increased FFA uptake. Only the phloretin-inhibitable component was increased by treatment, which normalized this activity in diabetic muscle cells. Under the same conditions, FFA oxidation was also increased by thiazolidinedione treatment. Increases in FFA uptake and oxidation were associated with upregulation of fatty acid translocase (FAT/CD36) expression. FAT/CD36 protein was increased by Tgz (90 ± 22% over control), Rgz (146 ± 42%), and Pio (111 ± 37%, P < 0.05 for all 3) treatment. Tgz treatment had no effect on fatty acid transporter protein-1 and membrane-associated plasmalemmal fatty acid-binding protein mRNA expression. We conclude that FFA uptake into cultured muscle cells is, in part, protein mediated and acutely insulin responsive. The basal activity of FFA uptake is impaired in type 2 diabetes. In addition, chronic thiazolidinedione treatment increased FFA uptake and oxidation into cultured human skeletal muscle cells in concert with upregulation of FAT/CD36 expression. Increased FFA uptake and oxidation may contribute to lower circulating FFA levels and reduced insulin resistance in skeletal muscle of individuals with type 2 diabetes following thiazolidinedione treatment.

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Section: Discussionmentioning

confidence: 77%

Thiazolidinediones upregulate impaired fatty acid uptake in skeletal muscle of type 2 diabetic subjects

Wilmsen

Ciaraldi

Carter

et al. 2003

American Journal of Physiology-Endocrinology and Metabolism

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show abstract

“…FAT/CD36 is one of several proteins that serve to facilitate the uptake and metabolism of extracellular long-chain fatty acids in muscle cells (33,34). PPAR-␥ stimulation facilitates fat cell differentiation and also stimulates fatty acid oxidation (35)(36)(37). Previous studies demonstrated that FAT/CD36 is a PPAR-␥ response gene because the FAT/CD36 mRNA increases after PPAR-␥ stimulation, and it seems possible that this protein participates in the differentiation and oxidative processes mediated by the activation of the PPAR-␥ receptor (38,39).…”

Section: Discussionmentioning

confidence: 99%

Thiazolidinedione Treatment Prevents Free Fatty Acid–Induced Insulin Resistance in Male Wistar Rats

Hevener

Reichart²,

Olefsky³

2001

Diabetes

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“…Presumably TZD-induced improvement in fatty acid trapping in adipose tissue would lead gradually to a reduction in acylglycerol content in other tissues. This has been shown in rats [88,89], although not yet tested in humans.…”

Section: Other Aspects Of This Hypothesismentioning

confidence: 91%

Adipose tissue as a buffer for daily lipid flux

2002

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Tissue-specific actions of antidiabetic thiazolidinediones on the reduced fatty acid oxidation in skeletal muscle and liver of zucker diabetic fatty rats

Cited by 39 publications

References 26 publications

Thiazolidinediones upregulate impaired fatty acid uptake in skeletal muscle of type 2 diabetic subjects

Thiazolidinediones upregulate impaired fatty acid uptake in skeletal muscle of type 2 diabetic subjects

Thiazolidinedione Treatment Prevents Free Fatty Acid–Induced Insulin Resistance in Male Wistar Rats

Adipose tissue as a buffer for daily lipid flux

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