PPAR-gamma gene expression is elevated in skeletal muscle of obese and type II diabetic subjects

Park, K. S.; Ciaraldi, T. P.; Abrams-Carter, L.; Mudaliar, S.; Nikoulina, Svetlana E.; Henry, R. R.

doi:10.2337/diabetes.46.7.1230

Cited by 42 publications

(35 citation statements)

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“…We have previously shown that insulin infusion rapidly increases PPARg mRNA expression in muscle [22]. That protein expression of any PPAR was not up-regulated after 3 h of insulin exposure could be due to translational kinetics which do not permit complete synthesis and processing of detectable additional quantities of the proteins in that time.…”

Section: Discussionmentioning

confidence: 99%

“…The majority of these observations were made in adipose tissue, yet PPARg action in skeletal muscle could differ from that in the adipocyte. We [22] and others [12,20,21] have identified PPARg mRNA in skeletal muscle, although in lower abundance than in adipose tissue and investigated its regulation and possible involvement in insulin action.…”

Section: Discussionmentioning

confidence: 99%

“…Relative intensities of transcript signals in the linear range were compared quantitatively using computer imaging (NIH Image). The mRNA for PPARg1,2 was measured by a quantitative reverse transcriptase-PCR assay, as described previously [22].…”

Section: Methodsmentioning

confidence: 99%

“…In previous studies from our laboratory, PPARg gene expression (mRNA) in skeletal muscle was found to be rapidly up-regulated in response to insulin treatment in both non-diabetic control and Type II diabetic subjects [22]. In the current report, other than comparing tissue distribution of PPARs in human muscle and fat, we sought to determine PPARa, PPARb and PPARg protein expression in the tissues of subjects with and without Type II diabetes.…”

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confidence: 99%

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Distribution of peroxisome proliferator-activated receptors (PPARs) in human skeletal muscle and adipose tissue: relation to insulin action

et al. 2000

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Distribution of peroxisome proliferator-activated receptors (PPARs) in human skeletal muscle and adipose tissue: relation to insulin action

et al. 2000

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“…The identification of PPAR-␥ in nonadipose tissues 25,26 has suggested novel functions for this receptor, distinct from its well-characterized metabolic regulatory activity. PPAR-␥ mRNA and protein were identified in rat aortic VSMCs, 27 as well as in human endothelial cells and VSMCs.…”

Section: Discussionmentioning

confidence: 99%

Increased Expression of Peroxisome Proliferator-Activated Receptor-α and -γ in Blood Vessels of Spontaneously Hypertensive Rats

Diep

Schiffrin

2001

Hypertension

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Abstract-Peroxisome proliferator-activated receptors (PPARs) are a family of ligand-activated transcription factors that include PPAR-␣, PPAR-␥, and PPAR-␦. We hypothesized that PPAR expression in blood vessels could be reduced in hypertension to result in increased vascular growth and reduced apoptosis. We investigated the abundance of PPAR-␣ and PPAR-␥ in aorta and mesenteric arteries from young (6-week-old) and adult (16-week-old) spontaneously hypertensive rats (SHR) compared with age-matched control Wistar-Kyoto rats (WKY). mRNA levels of PPAR-␣ and PPAR-␥ were determined by reverse transcription-polymerase chain reaction. Protein expression was evaluated by Western blot and by immunohistochemistry. PPAR-␥ was expressed in aortic and mesenteric vascular smooth muscle cells (VSMCs) from intact tissue and cultured cells. PPAR-␣ was expressed in intact vascular tissue but was almost undetectable in cultured VSMCs. In mesenteric arteries from adult SHR, PPAR-␣ and PPAR-␥ mRNA levels were significantly greater than in WKY (PϽ0.05). In aorta, PPAR-␣ mRNA was significantly (PϽ0.05) more abundant in adult (but not in young) SHR than in WKY, whereas there was no difference in PPAR-␥ mRNA between WKY and SHR. PPAR-␣ and PPAR-␥ mRNA were greater in mesenteric arteries (PϽ0.05) in young and adult SHR than in WKY. Expression of PPAR-␣ and PPAR-␥ was similar in SHR and WKY in other tissues. In cultured mesenteric VSMCs, PPAR-␥ mRNA was 3-fold higher in SHR than in WKY. Immunohistochemistry demonstrated that PPAR-␥ resided constitutively in the cytoplasm in primary and low-passaged aortic and mesenteric VSMCs, whereas PPAR-␣ was almost undetectable. Thus, aorta and mesenteric resistance arteries from SHR in the prehypertensive and the established phase of hypertension exhibit increased expression of both PPAR isoforms, whereas other tissues do not. Changes (increases) in PPAR expression may play a compensatory role in the remodeling of blood vessels in SHR.

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Modulation of PPARγ activity with pharmaceutical agents: Treatment of insulin resistance and atherosclerosis

Wang

Tafuri

2003

J of Cellular Biochemistry

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The anti-diabetic thiazolidinediones (TZDs) are a class of compounds with insulin-sensitizing activity that were originally discovered using in vivo pharmacological screens. In subsequent binding studies, TZDs were demonstrated to enhance insulin action by activating peroxisome proliferator-activated receptor gamma (PPARgamma). PPARgamma is a member of the ligand-activated nuclear receptor superfamily that promotes adipogenesis and enhances insulin sensitivity by controlling the expression of genes in glucose and lipid metabolism. Given the large size of the ligand binding pocket in PPARgamma, novel classes of both full and partial agonists that are structurally distinct from TZDs have been discovered. These compounds have been effective tools in differentiating adipogenic and insulin-sensitizing activities as well as tissue selectivity of PPARgamma activation. This information has led to the hypothesis that one ligand can activate or inactivate PPARs depending upon the tissue in which the PPAR resides. Thus particular compounds can be designated selective PPAR modulators or SPPARMs, a concept similar to that observed with the activation of estrogen receptor (ER) by SERMS. Additionally, both preclinical and clinical data suggest that PPARgamma activation is useful for the prevention of atherosclerosis. However, the effects of TZDs on plasma lipid profiles do not solely account for their anti-atherogenic effects. Recent studies with macrophage cells and animal models for atherosclerosis indicate that TZDs reduce the size and number of lesions formed in the vessel wall by modulating foam cell formation and inflammatory responses by macrophages. Thus in addition to the treatment of type II diabetes, PPARgamma agonists can be potentially employed for the treatment of atherosclerosis in general population.

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PPAR-gamma gene expression is elevated in skeletal muscle of obese and type II diabetic subjects

Cited by 42 publications

References 0 publications

Distribution of peroxisome proliferator-activated receptors (PPARs) in human skeletal muscle and adipose tissue: relation to insulin action

Distribution of peroxisome proliferator-activated receptors (PPARs) in human skeletal muscle and adipose tissue: relation to insulin action

Increased Expression of Peroxisome Proliferator-Activated Receptor-α and -γ in Blood Vessels of Spontaneously Hypertensive Rats

Modulation of PPARγ activity with pharmaceutical agents: Treatment of insulin resistance and atherosclerosis

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