Glycerolipid biosynthesis in rat adipose tissue. Influence of adipose-cell size and site of adipose tissue on triacylglycerol formation in lean and obese rats

Jamdar, Subhash C.

doi:10.1042/bj1700153

Cited by 40 publications

(24 citation statements)

References 24 publications

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“…Protein concentrations were measured by the method of Bradford (30 (31,32). In brief, mice fed a HFD for 10 weeks were anesthetized, and a liver slice was taken from each mouse.…”

Section: Methodsmentioning

confidence: 99%

Aryl Hydrocarbon Receptor Plays Protective Roles against High Fat Diet (HFD)-induced Hepatic Steatosis and the Subsequent Lipotoxicity via Direct Transcriptional Regulation of Socs3 Gene Expression

Wada

Sunaga

Miyata

et al. 2016

Journal of Biological Chemistry

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“…Protein concentrations were measured by the method of Bradford (30 (31,32). In brief, mice fed a HFD for 10 weeks were anesthetized, and a liver slice was taken from each mouse.…”

Section: Methodsmentioning

confidence: 99%

Aryl Hydrocarbon Receptor Plays Protective Roles against High Fat Diet (HFD)-induced Hepatic Steatosis and the Subsequent Lipotoxicity via Direct Transcriptional Regulation of Socs3 Gene Expression

Wada

Sunaga

Miyata

et al. 2016

Journal of Biological Chemistry

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“…De novo lipogenesis activities were determined by the incorporation of [ 14 C]acetate into the lipids (16). Rat primary hepatocytes were plated in medium 199 and cultured overnight at 37°C.…”

Section: Methodsmentioning

confidence: 99%

Atypical antipsychotic drugs perturb AMPK-dependent regulation of hepatic lipid metabolism

Park

Lee

et al. 2011

American Journal of Physiology-Endocrinology and Metabolism

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Oh KJ, Park J, Lee SY, Hwang I, Kim JB, Park TS, Lee HJ, Koo SH. Atypical antipsychotic drugs perturb AMPK-dependent regulation of hepatic lipid metabolism. Am J Physiol Endocrinol Metab 300: E624-E632, 2011. First published January 11, 2011; doi:10.1152/ajpendo.00502.2010.-Dysregulation of lipid metabolism is a key feature of metabolic disorder related to side effects of antipsychotic drugs. Here, we investigated the molecular mechanism by which second-generation atypical antipsychotic drugs (AAPDs) affect hepatic lipid metabolism in liver. AAPDs augmented hepatic lipid accumulation by activating expression of sterol regulatory element-binding protein (SREBP) transcription factors, with subsequent induction of downstream target genes involved in lipid and cholesterol synthesis in hepatocytes. We confirmed the direct involvement of SREBPs on AAPD-induced expression of lipogenic and cholesterogenic genes by utilization of adenovirus for dominant negative SREBP (Ad-SREBP-DN). Interestingly, AAPDs significantly decreased phosphorylation of AMPK␣ and expression of fatty acid oxidation genes. Treatment of constitutive active AMPK restored AAPD-mediated dysregulation of genes involved in both lipid synthesis and fatty acid oxidation. Moreover, AAPDs decreased transcriptional activity of PPAR␣, a critical transcriptional regulator for controlling hepatic fatty acid oxidation, via an AMPKdependent manner. Close investigations revealed that mutations at the known p38 MAPK phosphorylation sites (S6/12/21A), but not mutations at the putative AMPK␣ phosphorylation sites (S167/373/453A), block AAPD-dependent reduction of PPAR␣ transcriptional activity, suggesting that p38 MAPK might be also involved in the regulatory pathway as a downstream effector of AAPDs/AMPK. Taken together, these data suggest that AAPD-stimulated hepatic dysregulation of lipid metabolism could result from the inhibition of AMPK activity, and pharmaceutical means to potentiate AMPK activity would contribute to restore hepatic lipid homeostasis that occurs during AAPD treatment.adenosine 5=-monophosphate-activated protein kinase; sterol regulatory element-binding protein; peroxisome proliferator-activated receptor-␣ ATYPICAL ANTIPSYCHOTIC DRUGS (AAPDs) have been used in the pharmacological treatment of schizophrenia (1). Although the second-generation AAPDs are much potent than the classical antipsychotics, treatment of AAPDs could cause troublesome side effects, such as obesity, insulin resistance, dyslipidemia, abnormal glucose tolerance, and diabetes (5,11,23,36).Patients taking stable doses of clinically assigned olanzapine (OLZ) or clozapine (CLZ) have significantly higher fat mass, plasma insulin, glucose, triglyceride, and cholesterol levels (4, 5, 28). However, the exact molecular mechanism by which AAPDs lead to metabolic disorder remains unknown.Dysregulation of lipid metabolism is a critical instigator for the metabolic disorder. Recently, it has been reported that antipsychotic drugs such as OLZ and CLZ activate maturation of sterol regulator...

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“…For example, in rats, Jamdar et al [16] found higher rates of lipid formation using [14C]glycerol 3-phosphate,…”

Section: Introductionmentioning

confidence: 99%

Gene Expression Patterns in Visceral and Subcutaneous Adipose Depots in Rats are Linked to Their Morphologic Features

Palou

Priego

Sánchez

et al. 2009

Cell Physiol Biochem

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The aim was to characterize the expression pattern of genes involved in lipid metabolism in internal (retroperitoneal, mesenteric) and subcutaneous (inguinal) adipose tissue depots in rats and their relation with site-specific morphological- and metabolic-features. Gene expression by RT-qPCR, western blot and morphometric analyses were performed. Lipogenesis-related genes (PPARγ2, SREBP1c, ACC1, GPAT, LPL, CD36, GLUT4) showed higher mRNA levels in the retroperitoneal depot versus the mesenteric and the inguinal depots; the expression of PPARgamma;2, ACC1, CD36, and GLUT4 in the mesenteric depot was also higher than in the inguinal depot. HKII was similarly expressed in the retroperitoneal and mesenteric depots and higher than in the inguinal one. The expression of lipolysis-related genes (HSL, ATGL) was higher in the retroperitoneal than in the mesenteric and inguinal depots, while the expression of fatty-acid oxidation-related genes (PPARα, CPT1) was lower in the retroperitoneal depot compared with the mesenteric and the inguinal depots. Thus, a higher expression of lipogenesis- and lipolysis-related genes and lower expression of fatty-acid oxidation-related genes in internal depots (particularly in the retroperitoneal, which also presents the largest adipocyte size) can explain its higher triacylglyceride turnover rates and hence account for the differential behavior of fat depots in physiological situations and its involvement in obesity-linked metabolic disorders.

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Glycerolipid biosynthesis in rat adipose tissue. Influence of adipose-cell size and site of adipose tissue on triacylglycerol formation in lean and obese rats

Cited by 40 publications

References 24 publications

Aryl Hydrocarbon Receptor Plays Protective Roles against High Fat Diet (HFD)-induced Hepatic Steatosis and the Subsequent Lipotoxicity via Direct Transcriptional Regulation of Socs3 Gene Expression

Aryl Hydrocarbon Receptor Plays Protective Roles against High Fat Diet (HFD)-induced Hepatic Steatosis and the Subsequent Lipotoxicity via Direct Transcriptional Regulation of Socs3 Gene Expression

Atypical antipsychotic drugs perturb AMPK-dependent regulation of hepatic lipid metabolism

Gene Expression Patterns in Visceral and Subcutaneous Adipose Depots in Rats are Linked to Their Morphologic Features

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