Disorders of uric acid and lipid metabolism in type 2 diabetes as a mani festation of constutional metabolic phenotype (part 2)

Abstract

In order to assess the effect of certain constitutional factors on the production and excretion of uric acid (UA), 72 examined female type 2 diabetes (DM2) patients, were divided by the level of serum UA into 2 cohorts: normouricemia — NU, or hyperuricemia — HU. Patients were then divided into groups on the basis of the presence or absence of general and abdominal obesity (AO). In general 6 groups were formed, including 3 with obesity and 3 non-obese. In the groups with similar levels of uricemia, presence of obesity associated with higher levels of UA, higher degree of insulin resistance and insulinemia, and with increased triglycerides and LDL cholesterol and decreased HDL, compared with the corresponding indices in non-obese subjects. In obese patients we were able to reveal the hypouricisuric effect of the relatively high insulinemia, by identifying significantly higher index of fractional excretion of UA in group with AO compared to those in patients without AO. Analysis of the data allows us to suppose that due to the different phenotypes of DM2, in patients with obesity and in non-obese, may prevail different mechanisms of imbalance between formation and excretion of urates. According to our hypothesis, in DM2 with obesity and AO, overproduction of UA may be provoked by increased synthesis of purines and lipids due to relatively high levels of insulin. Fractional excretion of UA may be reduced as a result of insulin-induced enhanced reabsorption of urate, but the final serum level of UA depends on maintaining renal function. In DM2 without obesity, a leading role in stimulating of UA production can play activation of sympathetic nervous system, which stimulates the production of stress hormones — adrenalin, cortisol, and activation of contrinsulin catabolic processes, in particular of purines degradation of form UA.