Adenosine deaminase and body mass index in non-insulin-dependent diabetes mellitus

We studied 273 subjects with non-insulin-dependent diabetes mellitus (NIDDM ) from the population of Penne, Italy. A low proportion of the adenosine de aminase (ADA)*2 allele is observed in NIDDM subjects with a body mass index (BMI) of 25 kg/m(2) or less. On the contrary, a high proportion of this al lele is observed in NIDDM patients with a BMI higher than 34 kg/m(2). In th e intermediate BMI class, the proportion of ADA*2 alleles does not differ s ignificantly from that of normal subjects from the same population. No sign ificant effect on the relation between ADA and BMI has been observed for th e following variables:sex, age at the time of study, age at onset, therapy with insulin, and dyslipidemia. A borderline effect has been observed for t he duration of disease. Several lines of experimental evidence suggest that an excess of adenosine Al receptor activity may contribute to adiposity in NIDDM. ADA is a polymorphic enzyme that irreversibly deaminates adenosine to inosine, contributing to the regulation of intracellular and extracellul ar concentrations of adenosine. Since the activity of genotypes carrying th e ADA*2 allele is lower than that of the more common genotype ADA*1/*1, gen etic variability of the enzyme could contribute to degree of obesity in NID DM. Our data also support attempts to ameliorate the metabolic control of d iabetes through pharmacological modulation of adenosine receptors. Copyrigh t (C) 1999 by W.B. Saunders Company.