Clusterin (apolipoprotein J): wither link with diabetes and cardiometabolic risk?

Aronis, Konstantinos N.; Kim, Young–Bum; Mantzoros, Christos S.

doi:10.1016/j.metabol.2010.12.013

Cited by 11 publications

(6 citation statements)

References 20 publications

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“…Increased CLU levels are associated with T2DM, metabolic syndrome and cardiovascular diseases [44,45]. Kujiraoka et al [46] reported higher serum CLU levels in diabetes patients than in patients with myocardial infarction, chronic coronary artery disease, or diabetes combined with chronic coronary artery disease.…”

Section: Discussionmentioning

confidence: 99%

Glucagon-like peptide-1 levels and dipeptidyl peptidase-4 activity in type 2 diabetes

Şenyiğit

Tabak

Orhanoğlu

et al. 2017

CIM

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Section: Discussionmentioning

confidence: 99%

Glucagon-like peptide-1 levels and dipeptidyl peptidase-4 activity in type 2 diabetes

Şenyiğit

Tabak

Orhanoğlu

et al. 2017

CIM

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“…Excretion of uromodulin has been reported to be downregulated in diabetic nephropathy (24,47,48), and reduced excretion of specific uromodulin fragments has also been observed in other forms of CKD (22). Clusterin (apolipoprotein J) has been known to be associated in diabetes (49), and a number of papers have been published on the possible use of urinary clusterin concentration analysis in the assessment of proteinuria and renal function disorders (50,51). α-1-antitrypsin seems to be a good marker for the differentiation between DN case and control subjects (26), but for the early diagnosis of DN the amplitude levels are not significantly different in the progressors compared with nonprogressors.…”

Section: Discussionmentioning

confidence: 99%

Urinary Proteomics for Early Diagnosis in Diabetic Nephropathy

et al. 2012

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Diabetic nephropathy (DN) is a progressive kidney disease, a well-known complication of long-standing diabetes. DN is the most frequent reason for dialysis in many Western countries. Early detection may enable development of specific drugs and early initiation of therapy, thereby postponing/preventing the need for renal replacement therapy. We evaluated urinary proteome analysis as a tool for prediction of DN. Capillary electrophoresis–coupled mass spectrometry was used to profile the low–molecular weight proteome in urine. We examined urine samples from a longitudinal cohort of type 1 and 2 diabetic patients (n = 35) using a previously generated chronic kidney disease (CKD) biomarker classifier to assess peptides of collected urines for signs of DN. The application of this classifier to samples of normoalbuminuric subjects up to 5 years prior to development of macroalbuminuria enabled early detection of subsequent progression to macroalbuminuria (area under the curve [AUC] 0.93) compared with urinary albumin routinely used to determine the diagnosis (AUC 0.67). Statistical analysis of each urinary CKD biomarker depicted its regulation with respect to diagnosis of DN over time. Collagen fragments were prominent biomarkers 3–5 years before onset of macroalbuminuria. Before albumin excretion starts to increase, there is a decrease in collagen fragments. Urinary proteomics enables noninvasive assessment of DN risk at an early stage via determination of specific collagen fragments.

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“…(Endocrinology 155: 2089 -2101, 2014) C lusterin is a disulfide-linked heterodimeric glycoprotein composed of ␣-and ␤-subunits that is constitutively expressed in almost all mammalian tissues (1). Although a single gene encodes clusterin, 3 mRNA isoforms are translated into a variety of proteins that can be grouped into secreted and nuclear clusterin according to their localization (2,3). Clusterin forms a high-density lipoprotein (HDL) complex with apolipoprotein A-1 (ApoA1) and is also incorporated into the soluble terminal complement complex in the plasma (4).…”

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confidence: 99%

Deficiency of Clusterin Exacerbates High-Fat Diet-Induced Insulin Resistance in Male Mice

Kwon

Heo

et al. 2014

Endocrinology

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The present study examined the role of clusterin in insulin resistance in high fat-fed wild-type and clusterin knockout (KO) mice. The plasma levels of glucose and C-peptide and islet size were increased in clusterin KO mice after an 8-week high-fat diet. In an ip glucose tolerance test, the area under the curve for glucose was not different, whereas the area under the curve for insulin was higher in clusterin KO mice. In a hyperinsulinemic-euglycemic clamp, the clamp insulin levels were higher in clusterin KO mice after the high-fat diet. After adjusting for the clamp insulin levels, the glucose infusion rate, suppression of hepatic glucose production, and glucose uptake were lower in clusterin KO mice in the high fat-fed group. The plasma levels of clusterin and clusterin mRNA levels in the skeletal muscle and liver were increased by the high-fat diet. The mRNA levels of the antioxidant enzymes were lower, and the mRNA levels of nicotinamide adenine dinucleotide phosphate oxidase (NOX) 1 and cytokines and protein carbonylation were higher in the skeletal muscle and liver in clusterin KO mice after the high-fat diet. Palmitate-induced gene expressions of NOX1 and cytokines were higher in the primary cultured hepatocytes of clusterin KO mice compared with the wild-type mice. Clusterin inhibited the gene expression and reactive oxygen species generation by palmitate in the hepatocytes and C2C12. AKT phosphorylation by insulin was reduced in the hepatocytes of clusterin KO mice. These results suggest that clusterin plays a protective role against high-fat diet-induced insulin resistance through the suppression of oxidative stress and inflammation.

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Clusterin (apolipoprotein J): wither link with diabetes and cardiometabolic risk?

Cited by 11 publications

References 20 publications

Glucagon-like peptide-1 levels and dipeptidyl peptidase-4 activity in type 2 diabetes

Glucagon-like peptide-1 levels and dipeptidyl peptidase-4 activity in type 2 diabetes

Urinary Proteomics for Early Diagnosis in Diabetic Nephropathy

Deficiency of Clusterin Exacerbates High-Fat Diet-Induced Insulin Resistance in Male Mice

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