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 deaminase (ADA)*2 allele is observed in NIDDM subjects with a body mass index (BMI) of 25 kg/m2 or less. On the contrary, a high proportion of this allele is observed in NIDDM patients with a BMI higher than 34 kg/m2. In the intermediate BMI class, the proportion of ADA*2 alleles does not differ significantly from that of normal subjects from the same population. No significant effect on the relation between ADA and BMI has been observed for the following variables: sex, age at the time of study, age at onset, therapy with insulin, and dyslipidemia. A borderline effect has been observed for the duration of disease. Several lines of experimental evidence suggest that an excess of adenosine A1 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 extracellular concentrations of adenosine. Since the activity of genotypes carrying the ADA*2 allele is lower than that of the more common genotype ADA*1/*1, genetic variability of the enzyme could contribute to degree of obesity in NIDDM. Our data also support attempts to ameliorate the metabolic control of diabetes through pharmacological modulation of adenosine receptors.[1]References
- Adenosine deaminase and body mass index in non-insulin-dependent diabetes mellitus. Bottini, E., Gloria-Bottini, F. Metab. Clin. Exp. (1999) [Pubmed]
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