We are analyzing https://link.springer.com/article/10.1007/s00125-013-3095-6.

Title:
Liver X receptors preserve renal glomerular integrity under normoglycaemia and in diabetes in mice | Diabetologia
Description:
Aims/hypothesis Liver X receptors (LXRs) α and β are nuclear hormone receptors that are widely expressed in the kidney. They promote cholesterol efflux from cells and inhibit inflammatory responses by regulating gene transcription. Here, we hypothesised (1) that LXR deficiency would promote renal decline in a mouse model of diabetes by accelerating intraglomerular cholesterol accumulation and, conversely, (2) that LXR agonism would attenuate renal decline in diabetes. Methods Diabetes was induced with streptozotocin (STZ) and maintained for 14 weeks in Lxrα/β +/+ (Lxrα, also known as Nr1h3; Lxrβ, also known as Nr1h2) and Lxrα/β −/− mice. In addition, STZ-injected DBA/2J mice were treated with vehicle or the LXR agonist N,N-dimethyl-hydroxycholenamide (DMHCA) (80 mg/kg daily) for 10 weeks. To determine the role of cholesterol in diabetic nephropathy (DN), mice were placed on a Western diet after hyperglycaemia developed. Results Even in the absence of diabetes, Lxrα/β −/− mice exhibited a tenfold increase in the albumin:creatinine ratio and a 40-fold increase in glomerular lipid accumulation compared with Lxrα/β +/+ mice. When challenged with diabetes, Lxrα/β −/− mice showed accelerated mesangial matrix expansion and glomerular lipid accumulation, with upregulation of inflammatory and oxidative stress markers. In the DN-sensitive STZ DBA/2J mouse model, DMHCA treatment significantly decreased albumin and nephrin excretion (by 50% each), glomerular lipids and plasma triacylglycerol (by 70%) and cholesterol (by 48%); it also decreased kidney inflammatory and oxidative stress markers compared with vehicle-treated mice. Conclusions/interpretation These data support the idea that LXR plays an important role in the normal and diabetic kidney, while showing that LXR, through its inhibitory effect on inflammation and cholesterol accumulation in glomeruli, could also be a novel therapeutic target for DN.
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mice, lxrαβ, lxr, fig, diabetic, kidney, article, dmhca, google, scholar, pubmed, cholesterol, cas, renal, expression, compared, diabetes, lipid, stz, levels, accumulation, esm, data, glomerular, receptor, liver, increased, vehicle, lipids, gene, nephropathy, treatment, glomeruli, nondiabetic, inflammatory, mesangial, activation, cells, decreased, receptors, dbaj, increase, staining, matrix, protein, control, urinary, role, diet, stress,

Topics {✒️}

student–newman–keuls tests student–newman–keuls gov/grants/olaw/references/phspol stz-injected dba/2j mice cardiac renin–angiotensin–aldosterone system high-calorie/high-fat diet low-density lipoprotein-induced expression image analysis showed angiotensin ii-infused mice diabetic dba/2j mice stz dba/2j mice lxr-mediated ras-dependent actions nuclear hormone receptors diabetic lxrα/β +/+mice diabetic lxrα/β+/+ mice lxrα/β +/+ stz-treated brosius fc 3rd long-term renal outcomes matching wild-type mice systemic lxr activation 250 μl hplc-grade methanol lxrα/β +/+ 50 mg/kg lxrα/β −/− 35 mg/kg hyperglycemia-induced renal damage fluorescently labelled ox-ldl vehicle-treated diabetic mice stz-treated animals compared gene-selective lxr ligand rate-limiting enzyme involved receptor–alpha reduces activation reduces plaque formation α-smooth muscle actin streptozotocin-induced diabetic rats dba/2j mice lxr-dependent gene expression end-stage renal disease stz-injected mice dmhca-treated stz animals mice article published wild-type control group orphan nuclear receptors atp-binding cassette de boer ra diabetic mice treated dba/2j model diabetic lxrα/β +/+ diabetic lxrα/β −/− male lxrα/β −/− n-dimethyl-hydroxycholenamide dn preserving glomerular homeostasis

Questions {❓}

Orchard TJ, Chang YF, Ferrell RE, Petro N, Ellis DE (2002) Nephropathy in type 1 diabetes: a manifestation of insulin resistance and multiple genetic susceptibilities?

Schema {🗺️}

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      headline:Liver X receptors preserve renal glomerular integrity under normoglycaemia and in diabetes in mice
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         Internal Medicine
         Metabolic Diseases
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               type:PostalAddress
            type:Organization
            name:Banting and Best Diabetes Centre
            address:
               name:Banting and Best Diabetes Centre, Toronto, Canada
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Faculty of Pharmacy, University of Toronto, Toronto, Canada
      name:Division of Renal Diseases and Hypertension, Department of Medicine, University of Colorado, Aurora, USA
      name:VA Medical Center, Denver, USA
      name:Faculty of Pharmacy, University of Toronto, Toronto, Canada
      name:Department of Pathology, University Health Network, Toronto, Canada
      name:Faculty of Pharmacy, University of Toronto, Toronto, Canada
      name:Division of Renal Diseases and Hypertension, Department of Medicine, University of Colorado, Aurora, USA
      name:VA Medical Center, Denver, USA
      name:Division of Renal Diseases and Hypertension, Department of Medicine, University of Colorado, Aurora, USA
      name:VA Medical Center, Denver, USA
      name:Faculty of Pharmacy, University of Toronto, Toronto, Canada
      name:Division of Renal Diseases and Hypertension, Department of Medicine, University of Colorado, Aurora, USA
      name:VA Medical Center, Denver, USA
      name:Department of Chemistry, York University, Toronto, Canada
      name:Keenan Research Centre of the Li Ka Shing Knowledge Institute, St. Michael’s Hospital, Toronto, Canada
      name:Banting and Best Diabetes Centre, Toronto, Canada
      name:Division of Renal Diseases and Hypertension, Department of Medicine, University of Colorado, Aurora, USA
      name:VA Medical Center, Denver, USA
      name:Faculty of Pharmacy, University of Toronto, Toronto, Canada
      name:Banting and Best Diabetes Centre, Toronto, Canada

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