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PPARγ Agonist Improves Neuronal Insulin Receptor Function in Hippocampus and Brain Mitochondria Function in Rats with Insulin Resistance Induced by Long Term High-Fat Diets

Pipatpiboon, Noppamas, Pratchayasakul, Wasana, Chattipakorn, Nipon, Chattipakorn, Siriporn C.·2012·Endocrinology
DOI 10.1210/en.2011-1502
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Abstract

We previously demonstrated that a high-fat diet (HFD) consumption can cause not only peripheral insulin resistance, but also neuronal insulin resistance. Moreover, the consumption of an HFD has been shown to cause mitochondrial dysfunction in both the skeletal muscle and liver. Rosiglitazone, a peroxizome proliferator-activated receptor-γ ligand, is a drug used to treat type 2 diabetes mellitus. Recent studies suggested that rosiglitazone can improve learning and memory in both human and animal models. However, the effects of rosiglitazone on neuronal insulin resistance and brain mitochondria after the HFD consumption have not yet been investigated. Therefore, we tested the hypothesis that rosiglitazone improves neuronal insulin resistance caused by a HFD via attenuating the dysfunction of neuronal insulin receptors and brain mitochondria. Rosiglitazone (5 mg/kg · d) was given for 14 d to rats that were fed with either a HFD or normal diet for 12 wk. After the 14th week, all animals were euthanized, and their brains were removed and examined for insulin-induced long-term depression, neuronal insulin signaling, and brain mitochondrial function. We found that rosiglitazone significantly improved peripheral insulin resistance and insulin-induced long-term depression and increased neuronal Akt/PKB-ser phosphorylation in response to insulin. Furthermore, rosiglitazone prevented brain mitochondrial conformational changes and attenuated brain mitochondrial swelling, brain mitochondrial membrane potential changes, and brain mitochondrial ROS production. Our data suggest that neuronal insulin resistance and the impairment of brain mitochondria caused by a 12-wk HFD consumption can be reversed by rosiglitazone.

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  • The increase in Angptl4 in the hypothalamus of ob/ob type 2 diabetic mice is most likely due to insulin resistance.

    “The increase in Angplt4 in type 2 diabetes in hypothalamus of ob/ob mice is most likely due to insulin resistance, since we [37,38] and others [39,40] have shown, obesity is associated with increased inflammation and mitochondrial dysfunction at the level of the hypothalamus and both of these can contribute to an altered insulin response.”

    From Differential effects of angiopoietin-like 4 in brain and muscle on regulation of lipoprotein lipase activity (2015) · cites this paper as [40]

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Metadata

Authors
Pipatpiboon, N., Pratchayasakul, W., Chattipakorn, N., & Chattipakorn, S. C.
Affiliations
Neuroelectrophysiology Unit, Cardiac Electrophysiology Research and Training Center (N.P., W.P., N.C., S.C.C.), Chiang Mai 50200 Thailand
Venue
Endocrinology
Publisher
The Endocrine Society
Published
2012-01-01
Volume
153
Issue
1
Pages
329-338
ISSN
  • 0013-7227
  • 1945-7170
DOI
10.1210/en.2011-1502
Cited by
198
References
6
Language
en

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