Hyperlipidemia aggravates renal disease in B6.ROP Os/+ mice

Mühlfeld, Anja; Spencer, Min; Hudkins, Kelly L.; Kirk, Elizabeth A.; LeBoeuf, Renée C.; Alpers, Charles E.

doi:10.1111/j.1523-1755.2004.00854.x

Cited by 27 publications

(16 citation statements)

References 48 publications

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“…In this study we confi rm previous reports that hypercholesterolemia exacerbates diabetic nephropathy (17)(18)(19). However, our data expands on previous reports by including mice that had dietary manipulations of cholesterol consumption to determine the effect of changing dietary cholesterol on progression of diabetic nephropathy.…”

Section: Discussionsupporting

confidence: 65%

Reversibility of renal injury with cholesterol lowering in hyperlipidemic diabetic mice

Taneja

Thompson

Wilson

et al. 2010

Journal of Lipid Research

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Section: Discussionsupporting

confidence: 65%

Reversibility of renal injury with cholesterol lowering in hyperlipidemic diabetic mice

Taneja

Thompson

Wilson

et al. 2010

Journal of Lipid Research

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“…Photography, cell counting, quantitative measurements, and determination of semiquantitative parameters were performed on blinded slides. The following histological parameters were used to determine the glomerular changes (7,(21)(22)(23)(24): a) glomerular tuft/Bowman's capsule diameter ratio (three measurements of the glomerular tuft and of glomerulus plus Bowman's capsule diameters were taken for each and averaged, and the ratios were calculated); b) hypercellularity (determined by counting the number of nuclei in the glomerular tuft); c) integrity of Bowman's capsule visceral layer was determined; the coefficient of variation for three observers was 13.5 6 1%; d) morphology of glomerular capillaries was assessed semiquantitatively (0 5 normal, 1 5 dilated); the coefficient of variation for three observers was 9.5 6 1%; and e) PAS staining for mesangial area. Glomerular immunostaining for MCP-1 and for periglomerular F4/80 accumulation was quantified on 20-30 photographed glomerular cross sections per mouse after importing the images into Image Pro Plus software (Media Cybernetics, Silver Spring, MD).…”

Section: Morphometry and Associated Statistical Methodsmentioning

confidence: 99%

D-4F reduces EO6 immunoreactivity, SREBP-1c mRNA levels, and renal inflammation in LDL receptor-null mice fed a Western diet

Buga

Frank

Mottino

et al. 2008

Journal of Lipid Research

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LDL receptor-null (LDLR 2/2 ) mice on a Western diet (WD) develop endothelial dysfunction and atherosclerosis, which are improved by the apolipoprotein A-I (apoA-I) mimetic peptide D-4F. Focusing on the kidney, LDLR 2/2 mice were fed a WD with D-4F or the inactive control peptide scrambled D-4F (ScD-4F) added to their drinking water. The control mice (ScD-4F) developed glomerular changes, increased immunostaining for MCP-1/CCL2 chemokine, increased macrophage CD68 and F4/80 antigens, and increased oxidized phospholipids recognized by the EO6 monoclonal antibody in both glomerular and tublointerstitial areas. All of these parameters were significantly reduced by D-4F treatment, approaching levels found in wildtype C57BL/6J or LDLR 2/2 mice fed a chow diet. Sterolregulatory element binding protein-1c (SREBP-1c) mRNA levels and triglyceride levels were elevated in the kidneys of the control mice (ScD-4F) fed the WD compared with C57BL/6J and LDLR 2/2 mice on chow (P , 0.001 and P , 0.001, respectively) and compared with D-4F-treated mice on the WD (P , 0.01). There was no significant difference in plasma lipids, lipoproteins, glucose, blood pressure, or renal apoB levels between D-4F-and ScD-4F-treated mice. We conclude that D-4F reduced renal oxidized phospholipids, resulting in lower expression of SREBP-1c, which, in turn, resulted in lower triglyceride content and reduced renal inflammation. ) mice has been shown to induce atherosclerosis, endothelial dysfunction, and inflammation of brain arterioles associated with cognitive dysfunction, all of which have been reported to be significantly ameliorated by treatment with the oral apolipoprotein A-I (apoA-I) mimetic peptide D-4F without a change in plasma lipid levels or blood pressure (1-3).In addition to hyperlipidemia, feeding a WD to LDLR 2/2 mice results in insulin resistance and elevated plasma glucose levels (4, 5). A major problem facing Western societies is an increase in chronic renal disease that appears to be associated with dyslipidemia and diabetes in addition to hypertension (6). Dyslipidemia has been emphasized as a factor that can exacerbate hypertension-induced renal damage as well as a factor that by itself may have adverse effects on the kidney (6). Diet-induced obesity in C57BL/6J mice has been reported to cause lipid accumulation in kidneys and glomerulosclerosis via a sterol-regulatory element binding protein 1c (SREBP-1c)-dependent pathway (7). Oxidized phospholipids have been identified as potent mediators of inflammation (8,9). Berliner and colleagues have reported that oxidized phospholipids induce cytokine production in endothelial cells through induction of SREBP (10) via an endothelial nitric oxide synthase (eNOS)-mediated mechanism (11).Pritchard and colleagues reported that the apoA-I mimetic peptide L-4F (identical to D-4F except that the peptide is synthesized from L-amino acids) restored the balance between nitric oxide and superoxide anion production by eNOS in LDL-treated endothelial cells in culture (12). Injection of ...

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“…It is characterized by elevated serum total cholesterol, low density lipoprotein, very low density lipoprotein and decreased high density lipoprotein levels [11] though may be asymptomatic. Hyperlipidemia causes atherosclerotic cardiovascular disease which eventually affects organs such as the kidney, leading to glomerular injury, interstitial fibrosis and tubular atrophy, ischemic nephropathy and End Stage Renal Disease [12]. Increase in body weight and certain organs such as liver and spleen are also associated with hyperlipidemia due to increase in cholesterol and triglycerides and infiltration of these lipids to the organs respectively.…”

Section: Introductionmentioning

confidence: 99%

Effects of Garcinia kola biflavonoid fractions on serum lipid profile and kidney function parameters in hyperlipidemic rats

et al. 2016

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Background: Garcinia kola is used in traditional medicine in various parts of Africa including Nigeria for the amelioration of hypertension, cough, diabetes, sickle cell anemia, bacterial and fungal infections amongst others. The prophylactic and therapeutic efficacy of Garcinia kola biflavonoid fractions (GKBF); root bark (RBBF), stem bark (SBBF) and seed (SBF)) on the lipid profile and kidney function of Poloxamer 407 (P407) induced hyperlipidemic rats were determined.

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Hyperlipidemia aggravates renal disease in B6.ROP Os/+ mice

Abstract: This study demonstrates that hyperlipidemia worsens renal pathology in B6.ROP Os/+ mice with a decline in renal function mediated at least in part through increased renal expression of the cytokines PDGF B and TGF-beta.

Cited by 27 publications

References 48 publications

Reversibility of renal injury with cholesterol lowering in hyperlipidemic diabetic mice

Reversibility of renal injury with cholesterol lowering in hyperlipidemic diabetic mice

D-4F reduces EO6 immunoreactivity, SREBP-1c mRNA levels, and renal inflammation in LDL receptor-null mice fed a Western diet

Effects of Garcinia kola biflavonoid fractions on serum lipid profile and kidney function parameters in hyperlipidemic rats

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