Low Insulin-like Growth Factor-II Levels Predict Weight Gain in Normal Weight Subjects with Type 2 Diabetes

• Published in: The American journal of medicine Vol. 119; no. 2; pp. 167.e9 - 167.e15
• Main Authors: Heald, Adrian H., Kärvestedt, Lars, Anderson, Simon G., McLaughlin, Julie, Knowles, Anne, Wong, Louise, Grill, Valdemar, Cruickshank, J. Kennedy, White, Anne, Gibson, J. Martin, Brismar, Kerstin
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.02.2006
• Subjects: Body Mass Index; Diabetes Mellitus, Type 2 - blood; Diabetes Mellitus, Type 2 - diet therapy; Diabetes Mellitus, Type 2 - drug therapy; Follow-Up Studies; Humans; Hypoglycemic Agents - therapeutic use; IGF-II; Insulin - therapeutic use; Insulin-Like Growth Factor I - analysis; Insulin-Like Growth Factor II - analysis; Metformin - therapeutic use; Middle Aged; Sulfonylurea Compounds - therapeutic use; Type 2 diabetes; Weight Gain; Type 2 diabetes; Weight gain; IGF-II
• ISSN: 0002-9343; 1555-7162; 1555-7162
• DOI: 10.1016/j.amjmed.2005.08.001

Insulin-like growth factor (IGF)-I and IGF-II are important in the regulation of metabolism and growth. We previously reported in normoglycemic individuals of normal weight that low circulating IGF-II predicts future weight gain. We subsequently investigated whether such relationships persisted in circumstances of type 2 diabetes. In 224 subjects with type 2 diabetes we assessed the association between baseline IGF-II levels and risk of weight gain (>2.0 kg) at the 5-year follow-up. At follow-up, 90 participants (40.2%) gained more than 2.0 kg in body weight. For subjects (body mass index <26) at baseline, mean IGF-II levels were significantly lower in those who gained more than 2 kg in weight than in subjects of stable weight, 454 ng/mL (95% confidence interval 349-559) versus 620 ng/mL (534-705) (F = 7.4, P = .01). For this subgroup low circulating IGF-II at baseline strongly correlated with weight gain (Spearman rho = −0.52, P <.001). With increasing weight, the relationship no longer prevailed. Logistic regression showed that for body mass index less than 26, individuals at baseline for each 100 ng/mL increase in baseline IGF-II there was a 47% decreased risk of gaining 2.0 kg or more in weight. Adjustment for treatment group did not materially alter this relationship. There was no difference in baseline IGF-II by treatment group. There was no difference between the group with weight gain and the group with stable weight in those who additionally received insulin or sulfonylurea treatment in the 5 years between the baseline visit and the follow-up. In subjects of normal weight with type 2 diabetes, baseline IGF-II concentration is inversely related to future weight gain, independent of treatment effect, strengthening the putative role for IGF-II in regulating fat mass. We propose that IGF-II measurement has potential utility in this group for targeting such individuals for early intervention.