Intramyocellular Lipid Is Not Significantly Increased in Healthy Young Insulin Resistant First-Degree Relatives of Diabetic Subjects
- Adamandia D. Kriketos, PHD1,
- Gareth S. Denyer, PHD2,
- Campbell H. Thompson, MD, DPHIL3 and
- Lesley V. Campbell, MBBS, FRACP14
- 1Diabetes and Obesity Research Program, Garvan Institute of Medical Research, Sydney, Australia
- 2School of Molecular and Microbial Sciences, University of Sydney, Sydney, Australia
- 3Department of General Medicine, Flinders University of South Australia, Adelaide, Australia
- 4Diabetes Centre, St. Vincent’s Hospital, Sydney, Australia
- Address correspondence to Prof. Lesley V. Campbell, Diabetes and Obesity Research Program, Garvan Institute of Medical Research, 384 Victoria St., Darlinghurst, Sydney, NSW 2010, Australia. E-mail: l.campbell{at}garvan.org.au.
Insulin resistance is an early phenotypic feature of nondiabetic first-degree relatives of type 2 diabetic subjects (FDR) (1,2). While intramyocellular lipid (IMCL) is a marker of insulin resistance (3), how it develops is not completely understood. To study early defects accompanying insulin resistance, we characterized a population at high risk of type 2 diabetes (4,5). We studied young, healthy, sedentary, nonsmoking (age <45 years, BMI <36 kg/m2), normolipidemic, and normal glucose tolerant subjects. At-risk FDR subjects (14 female and 5 male) were compared with control subjects without family history of diabetes (12 female and 10 male).
To test the lipid supply hypothesis, we extended previous investigations in …
