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Dyslipidaemia is associated with testosterone, oestradiol and androgen receptor CAG repeat polymorphism in men with type 2 diabetes

Summary Objective  There is a high prevalence of low testosterone and dyslipidaemia in men with type 2 diabetes. The androgen receptor CAG repeat polymorphism (AR CAG) affects receptor transcriptional activity (the shorter repeats the more sensitive AR) and is associated with androgenic parameters a...

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Published in:Clinical endocrinology (Oxford) 2011-05, Vol.74 (5), p.624-630
Main Authors: Stanworth, R. D., Kapoor, D., Channer, K. S., Jones, T. H.
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creator Stanworth, R. D.
Kapoor, D.
Channer, K. S.
Jones, T. H.
description Summary Objective  There is a high prevalence of low testosterone and dyslipidaemia in men with type 2 diabetes. The androgen receptor CAG repeat polymorphism (AR CAG) affects receptor transcriptional activity (the shorter repeats the more sensitive AR) and is associated with androgenic parameters and obesity. This study describes the relationships between testosterone, AR CAG and serum lipids in men with type 2 diabetes. Design and Patients  Cross‐sectional study of men with type 2 diabetes in a District General Hospital Diabetes Centre. Measurements  Correlation between testosterone, AR CAG and serum lipids. Results  HDL cholesterol (HDL‐C) correlated with total testosterone (TT) (r = 0·251, P 
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D. ; Kapoor, D. ; Channer, K. S. ; Jones, T. H.</creator><creatorcontrib>Stanworth, R. D. ; Kapoor, D. ; Channer, K. S. ; Jones, T. H.</creatorcontrib><description>Summary Objective  There is a high prevalence of low testosterone and dyslipidaemia in men with type 2 diabetes. The androgen receptor CAG repeat polymorphism (AR CAG) affects receptor transcriptional activity (the shorter repeats the more sensitive AR) and is associated with androgenic parameters and obesity. This study describes the relationships between testosterone, AR CAG and serum lipids in men with type 2 diabetes. Design and Patients  Cross‐sectional study of men with type 2 diabetes in a District General Hospital Diabetes Centre. Measurements  Correlation between testosterone, AR CAG and serum lipids. Results  HDL cholesterol (HDL‐C) correlated with total testosterone (TT) (r = 0·251, P &lt; 0·001), bioavailable testosterone (BT) (r = 0·19, P = 0·001), free testosterone (FT) (r = 0·165, P = 0·005) and sex hormone‐binding globulin (SHBG) (r = 0·147, P = 0·014). HDL‐C did not correlate with oestradiol, but men with the lowest quartile of oestradiol had lower HDL‐C compared to highest quartile (P = 0·046). Triglycerides correlated negatively with TT (r = −0·195, P = 0·001), BT (r = −0·148, P = 0·013) and SHBG (−0·14, P = 0·019) but not with FT or oestradiol. Total and LDL cholesterol (LDL‐C) correlated negatively with oestradiol (r = −0·121, P = 0·05) but not with testosterone or SHBG. One‐way anova testing across four quartiles of AR CAG showed a trend to alteration in HDL‐C across groups of AR CAG (P = 0·08). HDL‐C was significantly higher in men with the longest AR CAG compared with the shortest (1·19 vs 1·08 mmol/l, P = 0·02). Conclusions  Lower testosterone and oestradiol levels in men with diabetes are associated with an adverse lipid profile. Shorter AR CAG is associated with low HDL‐C and testosterone. The paradox that HDL‐C is associated with low testosterone levels and a more active AR may suggest divergent effect of testosterone on HDL‐C via genomic vs nongenomic mechanisms.</description><identifier>ISSN: 0300-0664</identifier><identifier>EISSN: 1365-2265</identifier><identifier>DOI: 10.1111/j.1365-2265.2011.03969.x</identifier><identifier>PMID: 21470285</identifier><identifier>CODEN: CLECAP</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Aged ; Biological and medical sciences ; Cholesterol, HDL - blood ; Cross-Sectional Studies ; Diabetes Mellitus, Type 2 - genetics ; Diabetes Mellitus, Type 2 - metabolism ; Diabetes Mellitus, Type 2 - physiopathology ; Diabetes. Impaired glucose tolerance ; Dyslipidemias - etiology ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Estradiol - blood ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Fundamental and applied biological sciences. Psychology ; Humans ; Male ; Medical sciences ; Middle Aged ; Polymorphism, Genetic ; Receptors, Androgen - genetics ; Testosterone - blood ; Trinucleotide Repeats ; Vertebrates: endocrinology</subject><ispartof>Clinical endocrinology (Oxford), 2011-05, Vol.74 (5), p.624-630</ispartof><rights>2011 Blackwell Publishing Ltd</rights><rights>2015 INIST-CNRS</rights><rights>2011 Blackwell Publishing Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4159-c939dff115f364e959eeefb544964302c881f93292673db3473e58b65e256a0a3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=24030520$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21470285$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Stanworth, R. D.</creatorcontrib><creatorcontrib>Kapoor, D.</creatorcontrib><creatorcontrib>Channer, K. S.</creatorcontrib><creatorcontrib>Jones, T. H.</creatorcontrib><title>Dyslipidaemia is associated with testosterone, oestradiol and androgen receptor CAG repeat polymorphism in men with type 2 diabetes</title><title>Clinical endocrinology (Oxford)</title><addtitle>Clin Endocrinol (Oxf)</addtitle><description>Summary Objective  There is a high prevalence of low testosterone and dyslipidaemia in men with type 2 diabetes. The androgen receptor CAG repeat polymorphism (AR CAG) affects receptor transcriptional activity (the shorter repeats the more sensitive AR) and is associated with androgenic parameters and obesity. This study describes the relationships between testosterone, AR CAG and serum lipids in men with type 2 diabetes. Design and Patients  Cross‐sectional study of men with type 2 diabetes in a District General Hospital Diabetes Centre. Measurements  Correlation between testosterone, AR CAG and serum lipids. Results  HDL cholesterol (HDL‐C) correlated with total testosterone (TT) (r = 0·251, P &lt; 0·001), bioavailable testosterone (BT) (r = 0·19, P = 0·001), free testosterone (FT) (r = 0·165, P = 0·005) and sex hormone‐binding globulin (SHBG) (r = 0·147, P = 0·014). HDL‐C did not correlate with oestradiol, but men with the lowest quartile of oestradiol had lower HDL‐C compared to highest quartile (P = 0·046). Triglycerides correlated negatively with TT (r = −0·195, P = 0·001), BT (r = −0·148, P = 0·013) and SHBG (−0·14, P = 0·019) but not with FT or oestradiol. Total and LDL cholesterol (LDL‐C) correlated negatively with oestradiol (r = −0·121, P = 0·05) but not with testosterone or SHBG. One‐way anova testing across four quartiles of AR CAG showed a trend to alteration in HDL‐C across groups of AR CAG (P = 0·08). HDL‐C was significantly higher in men with the longest AR CAG compared with the shortest (1·19 vs 1·08 mmol/l, P = 0·02). Conclusions  Lower testosterone and oestradiol levels in men with diabetes are associated with an adverse lipid profile. Shorter AR CAG is associated with low HDL‐C and testosterone. The paradox that HDL‐C is associated with low testosterone levels and a more active AR may suggest divergent effect of testosterone on HDL‐C via genomic vs nongenomic mechanisms.</description><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Cholesterol, HDL - blood</subject><subject>Cross-Sectional Studies</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Diabetes Mellitus, Type 2 - physiopathology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Dyslipidemias - etiology</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Estradiol - blood</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Polymorphism, Genetic</subject><subject>Receptors, Androgen - genetics</subject><subject>Testosterone - blood</subject><subject>Trinucleotide Repeats</subject><subject>Vertebrates: endocrinology</subject><issn>0300-0664</issn><issn>1365-2265</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNpdkU1v1DAQhi0EokvhLyBLCHEhwd8bHzi027IglYJQEVIvlpNMqJckDnZW3Zz54zjsskhYsuzRPO-MPS9CmJKcpvVmk1OuZMaYkjkjlOaEa6Xz3QO0OCYeogXhhGREKXGCnsS4IYTIgiwfoxNGxZKwQi7Qr4sptm5wtYXOWewitjH6ytkRanzvxjs8Qhx9HCH4Hl5jn6Jga-dbbPt63sF_hx4HqGAYfcCrs3UKBrAjHnw7dT4Mdy522PW4S9y-5DQAZrh2toRU_il61Ng2wrPDeYq-vru8Wb3Prj6tP6zOrrJKUKmzSnNdNw2lsuFKgJYaAJpSCqGV4IRVRUEbzZlmasnrkoslB1mUSgKTyhLLT9Grfd0h-J_b9BHTuVhB29oe_DaaQlFGJBUkkS_-Izd-G_r0OEOlkEVRME4T9fxAbcsOajME19kwmb_TTcDLA2BjZdsm2L5y8R-XOhHJ5nZv99y9a2E65ikxs9tmY2ZTzWyqmd02f9w2O7O6vJ5vSZ_t9S75tDvqbfhh0iiW0ny7XpuL24_6882Xc3PLfwMtbax6</recordid><startdate>201105</startdate><enddate>201105</enddate><creator>Stanworth, R. D.</creator><creator>Kapoor, D.</creator><creator>Channer, K. S.</creator><creator>Jones, T. H.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7QP</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>201105</creationdate><title>Dyslipidaemia is associated with testosterone, oestradiol and androgen receptor CAG repeat polymorphism in men with type 2 diabetes</title><author>Stanworth, R. D. ; Kapoor, D. ; Channer, K. S. ; Jones, T. H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4159-c939dff115f364e959eeefb544964302c881f93292673db3473e58b65e256a0a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Cholesterol, HDL - blood</topic><topic>Cross-Sectional Studies</topic><topic>Diabetes Mellitus, Type 2 - genetics</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Diabetes Mellitus, Type 2 - physiopathology</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Dyslipidemias - etiology</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Estradiol - blood</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Polymorphism, Genetic</topic><topic>Receptors, Androgen - genetics</topic><topic>Testosterone - blood</topic><topic>Trinucleotide Repeats</topic><topic>Vertebrates: endocrinology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Stanworth, R. D.</creatorcontrib><creatorcontrib>Kapoor, D.</creatorcontrib><creatorcontrib>Channer, K. S.</creatorcontrib><creatorcontrib>Jones, T. H.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Nursing &amp; Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical endocrinology (Oxford)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Stanworth, R. D.</au><au>Kapoor, D.</au><au>Channer, K. S.</au><au>Jones, T. H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dyslipidaemia is associated with testosterone, oestradiol and androgen receptor CAG repeat polymorphism in men with type 2 diabetes</atitle><jtitle>Clinical endocrinology (Oxford)</jtitle><addtitle>Clin Endocrinol (Oxf)</addtitle><date>2011-05</date><risdate>2011</risdate><volume>74</volume><issue>5</issue><spage>624</spage><epage>630</epage><pages>624-630</pages><issn>0300-0664</issn><eissn>1365-2265</eissn><coden>CLECAP</coden><abstract>Summary Objective  There is a high prevalence of low testosterone and dyslipidaemia in men with type 2 diabetes. The androgen receptor CAG repeat polymorphism (AR CAG) affects receptor transcriptional activity (the shorter repeats the more sensitive AR) and is associated with androgenic parameters and obesity. This study describes the relationships between testosterone, AR CAG and serum lipids in men with type 2 diabetes. Design and Patients  Cross‐sectional study of men with type 2 diabetes in a District General Hospital Diabetes Centre. Measurements  Correlation between testosterone, AR CAG and serum lipids. Results  HDL cholesterol (HDL‐C) correlated with total testosterone (TT) (r = 0·251, P &lt; 0·001), bioavailable testosterone (BT) (r = 0·19, P = 0·001), free testosterone (FT) (r = 0·165, P = 0·005) and sex hormone‐binding globulin (SHBG) (r = 0·147, P = 0·014). HDL‐C did not correlate with oestradiol, but men with the lowest quartile of oestradiol had lower HDL‐C compared to highest quartile (P = 0·046). Triglycerides correlated negatively with TT (r = −0·195, P = 0·001), BT (r = −0·148, P = 0·013) and SHBG (−0·14, P = 0·019) but not with FT or oestradiol. Total and LDL cholesterol (LDL‐C) correlated negatively with oestradiol (r = −0·121, P = 0·05) but not with testosterone or SHBG. One‐way anova testing across four quartiles of AR CAG showed a trend to alteration in HDL‐C across groups of AR CAG (P = 0·08). HDL‐C was significantly higher in men with the longest AR CAG compared with the shortest (1·19 vs 1·08 mmol/l, P = 0·02). Conclusions  Lower testosterone and oestradiol levels in men with diabetes are associated with an adverse lipid profile. Shorter AR CAG is associated with low HDL‐C and testosterone. The paradox that HDL‐C is associated with low testosterone levels and a more active AR may suggest divergent effect of testosterone on HDL‐C via genomic vs nongenomic mechanisms.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>21470285</pmid><doi>10.1111/j.1365-2265.2011.03969.x</doi><tpages>7</tpages></addata></record>
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ispartof Clinical endocrinology (Oxford), 2011-05, Vol.74 (5), p.624-630
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source Wiley-Blackwell Read & Publish Collection
subjects Aged
Biological and medical sciences
Cholesterol, HDL - blood
Cross-Sectional Studies
Diabetes Mellitus, Type 2 - genetics
Diabetes Mellitus, Type 2 - metabolism
Diabetes Mellitus, Type 2 - physiopathology
Diabetes. Impaired glucose tolerance
Dyslipidemias - etiology
Endocrine pancreas. Apud cells (diseases)
Endocrinopathies
Estradiol - blood
Etiopathogenesis. Screening. Investigations. Target tissue resistance
Fundamental and applied biological sciences. Psychology
Humans
Male
Medical sciences
Middle Aged
Polymorphism, Genetic
Receptors, Androgen - genetics
Testosterone - blood
Trinucleotide Repeats
Vertebrates: endocrinology
title Dyslipidaemia is associated with testosterone, oestradiol and androgen receptor CAG repeat polymorphism in men with type 2 diabetes
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