Rosiglitazone, a PPAR<i>γ</i> agonist, ameliorates palmitate‐induced insulin resistance and apoptosis in skeletal muscle cells

Meshkani, Reza; Sadeghi, Asie; Taheripak, Gholamreza; Zarghooni, Maryam; Gerayesh-Nejad, Siavash; Bakhtiyari, Salar

doi:10.1002/cbf.3072

Cited by 25 publications

(21 citation statements)

References 60 publications

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“…Because previous studies have reported that palmitate induces apoptosis in various cell types [16][17][18], we first determined the appropriate dose of palmitate for inducing apoptosis in HepG2 cells. The results of the MTT assay revealed that lower than 0.5mM of palmitate did not significantly suppressed the viability of HepG2 cells (Fig.…”

Section: Palmitate Decreases Cell Viability and Induces Apoptosis In mentioning

confidence: 99%

Inhibition of SH2-domain-containing inositol 5-phosphatase (SHIP2) ameliorates palmitate induced-apoptosis through regulating Akt/FOXO1 pathway and ROS production in HepG2 cells

Gorgani‐Firuzjaee

Adeli

Meshkani

2015

Biochemical and Biophysical Research Communications

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Section: Palmitate Decreases Cell Viability and Induces Apoptosis In mentioning

confidence: 99%

Inhibition of SH2-domain-containing inositol 5-phosphatase (SHIP2) ameliorates palmitate induced-apoptosis through regulating Akt/FOXO1 pathway and ROS production in HepG2 cells

Gorgani‐Firuzjaee

Adeli

Meshkani

2015

Biochemical and Biophysical Research Communications

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“…These changes suggest that PPARγ upregulation of SCD-1 resulted in elevated lipogenesis and strengthened adiponectin signaling. Further studies indicated that PPARγ agonists weaken palmitate-induced endoplasmic reticulum stress and apoptosis by SCD-1 generation (80–82). SCD-1 upregulation may lead to the lessening of cardiovascular disturbances through therapy with PPARγ agonists (81).…”

Section: Discussionmentioning

confidence: 99%

Thiazolidinedione induces a therapeutic effect on hepatosteatosis by regulating stearoyl‑CoA desaturase‑1, lipase activity, leptin and resistin

Al‐Muzafar

Amin

2018

Exp Ther Med

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Hepatosteatosis is a disease present worldwide, which presents a number of health problems. Recently, thiazolidinedione (TZD) has been used as a therapy for lipid disorders. The present study demonstrates the potential of TZD as a treatment for hepatosteatosis and its mechanism of action, particularly focusing on its role in lipid metabolism. A total of 60 (80–90 g) rats were divided into three groups: A normal group with a standard diet, a high-fat, high-carbohydrate diet (HFCD) group or a HFCD+TZD group (n=20/group). The HFCD induced hepatosteatosis over a period of 12 weeks and the HFCD+TZD group were administered TZD in weeks 13–16. Blood and tissue samples were collected to measure hepatic function, the lipid profile, metabolism and hormone biomarkers, including serum triglyceride (TG), lipoprotein lipase (LPL), stearoyl-CoA desaturase (SCD-1), leptin and resistin. The HFCD-fed rats exhibited a significant increase in serum TG, total cholesterol, low-density lipoproteins, alanine transaminase and bilirubin compared with the normal group as well as a significant decrease in high-density lipoprotein. In addition, serum leptin and resistin were significantly elevated in the HFCD group compared with the normal group. The administration of TZD significantly increased SCD-1 activity and significantly inhibited LPL activity. It also attenuated the changes in the lipid profiles and normalized serum leptin and resistin levels. The results of the present study indicated that HFCD induced lipid abnormalities associated with hypertriglyceridemia, hypercholesterolemia and hepatosteatosis. These changes resulted from disruption to leptin and resistin, which may be due to alterations in LPL and SCD-1 activity. TZD mitigated the effects of HFCD-induced hepatosteatosis, indicating a possible regulatory effect of TZD in the development of hepatosteatosis. The authors suggest that the manipulation of SCD-1 and lipase by TZD may be useful as a treatment for hepatosteatosis.

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“…These conditions are detrimental for cellular function and may eventually lead to cell death. Apoptosis has been shown to occur in skeletal muscle cells exposed to saturated palmitic acid [4,5]. Although various mechanisms may be involved, changes in mitochondrial respiration seem to play a central role in FFA-induced cellular damage (reviewed Abstract Unsaturated free fatty acids (FFA) are able to prevent deleterious effects of saturated FFA in skeletal muscle cells although the mechanisms involved are still not completely understood.…”

Section: Introductionmentioning

confidence: 99%

Protective Effect of Unsaturated Fatty Acids on Palmitic Acid‐Induced Toxicity in Skeletal Muscle Cells is not Mediated by PPARδ Activation

Tůmová

Mališová

Andĕl

et al. 2015

Lipids

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Unsaturated free fatty acids (FFA) are able to prevent deleterious effects of saturated FFA in skeletal muscle cells although the mechanisms involved are still not completely understood. FFA act as endogenous ligands of peroxisome proliferator-activated receptors (PPAR), transcription factors regulating the expression of genes involved in lipid metabolism. The aim of this study was to determine whether activation of PPARδ, the most common PPAR subtype in skeletal muscle, plays a role in mediating the protective effect of unsaturated FFA on saturated FFA-induced damage in skeletal muscle cells and to examine an impact on mitochondrial respiration. Mouse C2C12 myotubes were treated for 24 h with different concentrations of saturated FFA (palmitic acid), unsaturated FFA (oleic, linoleic and α-linolenic acid), and their combinations. PPARδ agonist GW501516 and antagonist GSK0660 were also used. Both mono- and polyunsaturated FFA, but not GW501516, prevented palmitic acid-induced cell death. Mono- and polyunsaturated FFA proved to be effective activators of PPARδ compared to saturated palmitic acid; however, in combination with palmitic acid their effect on PPARδ activation was blocked and stayed at the levels observed for palmitic acid alone. Unsaturated FFA at moderate physiological concentrations as well as GW501516, but not palmitic acid, mildly uncoupled mitochondrial respiration. Our results indicate that although unsaturated FFA are effective activators of PPARδ, their protective effect on palmitic acid-induced toxicity is not mediated by PPARδ activation and subsequent induction of lipid regulatory genes in skeletal muscle cells. Other mechanisms, such as mitochondrial uncoupling, may underlie their effect.

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Rosiglitazone, a PPARγ agonist, ameliorates palmitate‐induced insulin resistance and apoptosis in skeletal muscle cells

Cited by 25 publications

References 60 publications

Inhibition of SH2-domain-containing inositol 5-phosphatase (SHIP2) ameliorates palmitate induced-apoptosis through regulating Akt/FOXO1 pathway and ROS production in HepG2 cells

Inhibition of SH2-domain-containing inositol 5-phosphatase (SHIP2) ameliorates palmitate induced-apoptosis through regulating Akt/FOXO1 pathway and ROS production in HepG2 cells

Thiazolidinedione induces a therapeutic effect on hepatosteatosis by regulating stearoyl‑CoA desaturase‑1, lipase activity, leptin and resistin

Protective Effect of Unsaturated Fatty Acids on Palmitic Acid‐Induced Toxicity in Skeletal Muscle Cells is not Mediated by PPARδ Activation

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