Composition of insulin-induced body weight gain in diabetic patients: A bio-impedance study

Citation
V. Rigalleau et al., Composition of insulin-induced body weight gain in diabetic patients: A bio-impedance study, DIABETE MET, 25(4), 1999, pp. 321-328
Citations number
25
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
DIABETES & METABOLISM
ISSN journal
12623636 → ACNP
Volume
25
Issue
4
Year of publication
1999
Pages
321 - 328
Database
ISI
SICI code
1262-3636(199909)25:4<321:COIBWG>2.0.ZU;2-V
Abstract
Although insulin is a well-known cause of body weight gain, it is not clear whether it is due to the accumulation of fat or lean mass. We performed a 3 months Body-impedance Analysis follow-up in 72 diabetic patients in a wid e range of insulin indications: insulin introduction in young inaugural typ e 1 diabetics (n = 12), late-onset type 1 (n = 12), type 2 affected by inte rcurrent diseases (n = 12) or microangiopathic complications (n = 12), type 2 with failure of oral antidiabetic agents (n = 12), and insulin withdrawa l in type 2 (n = 12). In type 1 patients, insulin led to the most important weight gain, but it was fat-free, with a major benefit an HbA1C. Type 2 pa tients affected by intercurrent diseases or microangiopathic complications had a mild, also fat-free weight gain, with a clear benefit an HhA1C. In ty pe 2 patients with failure of oral agents, HbA1C declined less, weight gain was intermediar, but predominantly fat mirrored by a predominant fat loss in type 2 patients whose insulin was stopped (without significant change in HbA1C). Both fat and lean mass contributed to insulin-induced body weight gain, but a significant negative relationship existed between their respect ive evolution in our patients (r = -0.23, p < 0.05 by linear regression ana lysis between n fat mass and n lean mass). insulin-induced body weight gain is not univocal: insulin restaures or protects lean mass in its less contr oversial indications, whereas it leads to fat accumulation in type 2 patien ts with isolated failure of oral agents.