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
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.