scholarly journals Diet-induced Obesity in C57BL/6J Mice Causes Increased Renal Lipid Accumulation and Glomerulosclerosis via a Sterol Regulatory Element-binding Protein-1c-dependent Pathway

2005 ◽  
Vol 280 (37) ◽  
pp. 32317-32325 ◽  
Author(s):  
Tao Jiang ◽  
Zhuowei Wang ◽  
Gregory Proctor ◽  
Shevie Moskowitz ◽  
Scott E. Liebman ◽  
...  
Keyword(s):  
Lipid Accumulation ◽  
Binding Protein ◽  
Regulatory Element ◽  
Diet Induced Obesity ◽  
Element Binding Protein ◽  
Sterol Regulatory Element ◽  
Dependent Pathway

Chronic exercise provides renal-protective effects with upregulation of fatty acid oxidation in the kidney of high fructose-fed rats

2020 ◽  
Vol 318 (3) ◽  
pp. F826-F834
Author(s):  
Gaizun Hu ◽  
Lusi Xu ◽  
Yixuan Ma ◽  
Masahiro Kohzuki ◽  
Osamu Ito
Keyword(s):  
Renal Function ◽  
Fatty Acid ◽  
Lipid Accumulation ◽  
Binding Protein ◽  
Regulatory Element ◽  
High Fructose ◽  
Element Binding Protein ◽  
Sterol Regulatory Element ◽  
Acyl Coa Oxidase ◽  
Renal Expression

Excessive fructose intake causes metabolic syndrome and lipid accumulation in the kidney and leads to renal dysfunction and damage. Exercise (Ex) improves lipids regulation, but the mechanisms are unclarified in the kidney. In the present study, male Sprague-Dawley rats were allocated to groups fed with control or high-fructose (HFr) diet. Part of rats in each group underwent aerobic treadmill Ex for 12 wk. Drug treatment was performed as the fenofibrate gavage during the last 4 wk on HFr diet-fed rats. Renal function, histological changes, and expression of regulators involved in fatty acid (FA) metabolism were assessed. In CON diet-fed groups, Ex did not affect renal function or histology and significantly increased renal expression of FA β-oxidation regulators including acyl-CoA dehydrogenases (CADs), acyl-CoA oxidase, peroxisome proliferator-activated receptor (PPAR)-α, and PPAR-γ coactivator (PGC)-1α and lipogenic factors including acetyl-CoA carboxylase (ACCα), FA synthase (FAS), and sterol regulatory element-binding protein 1c. HFr caused albuminuria, lipid accumulation, and renal pathohistological changes, which were attenuated by Ex but not by fenofibrate. HFr decreased renal expression of medium- and short-chain CADs and PPAR-α and increased renal expression of ACCα, FAS, and sterol regulatory element-binding protein 1c. Ex increased expression of CADs, carnitine palmitoyltransferase type I, acyl-CoA oxidase, PPAR-α, and PGC-1α and decreased renal expression of ACCα and FAS in HFr diet-fed rats. The Ex-induced FA metabolism alteration was similar to that in the fenofibrate-treated group. In conclusion, the present study indicates that Ex enhanced renal FA metabolism, which might protect the kidney in lipid dysregulation diseases.

Resistance to high-fat diet-induced obesity and altered expression of adipose-specific genes in HSL-deficient mice

2003 ◽  
Vol 285 (6) ◽  
pp. E1182-E1195 ◽  
Author(s):  
Kenji Harada ◽  
Wen-Jun Shen ◽  
Shailja Patel ◽  
Vanita Natu ◽  
Jining Wang ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Insulin Receptor ◽  
Binding Protein ◽  
Regulatory Element ◽  
Mrna Levels ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Element Binding Protein ◽  
Sterol Regulatory Element ◽  
Adipose Differentiation

To elucidate the role of hormone-sensitive lipase (HSL) in diet-induced obesity, HSL-deficient ( HSL– /–) and wild-type mice were fed normal chow or high-fat diets. HSL– /– mice were resistant to diet-induced obesity showing higher core body temperatures. Weight and triacylglycerol contents were decreased in white adipose tissue (WAT) but increased in both brown adipose tissue (BAT) and liver of HSL– /– mice. Serum insulin levels in the fed state and tumor necrosis factor-α mRNA levels in adipose tissues were higher, whereas serum levels of adipocyte complement-related protein of 30 kDa (ACRP30)/adiponectin and leptin, as well as mRNA levels of ACRP30/adiponectin, leptin, resistin, and adipsin in WAT, were lower in HSL– /– mice than in controls. Expression of transcription factors associated with adipogenesis (peroxisome proliferator-activated receptor-γ, CAAT/enhancer-binding protein-α) and lipogenesis (carbohydrate response element-binding protein, adipocyte determination- and differentiation-dependent factor-1/sterol regulatory element-binding protein-1c), as well as of adipose differentiation markers (adipocyte lipid-binding protein, perilipin, lipoprotein lipase), lipogenic enzymes (glycerol-3-phosphate acyltransferase, acyl-CoA:diacylglycerol acyltransferase-1 and -2, fatty acid synthase, ATP citrate lyase) and insulin signaling proteins (insulin receptor, insulin receptor substrate-1, GLUT4), was suppressed in WAT but not in BAT of HSL– /– mice. In contrast, expression of genes associated with cholesterol metabolism (sterol-regulatory element-binding protein-2, 3-hydroxy-3-methylglutaryl-CoA reductase, acyl-CoA:cholesterol acyltransferase-1) and thermogenesis (uncoupling protein-2) was upregulated in both WAT and BAT of HSL– /– mice. Our results suggest that impaired lipolysis in HSL deficiency affects lipid metabolism through alterations of adipose differentiation and adipose-derived hormone levels.

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