Stepwise increase in plasma insulin and C-peptide concentrations in obese, in obese hypertensive, and in obese hypertensive diabetic subjects.

Several clinical and epidemiological evidences support the increased risk of cardiovascular disease (CVD) in pathological conditions as obesity, hypertension, non-insulin-dependent diabetes mellitus, which have hyperinsulinemia as a common feature. In this study, we assessed basal plasma insulin (IRI) and C-peptide (CPR) concentrations in 297 volunteers who participated in a survey concerning risk factors of CVD. We found a stepwise increase in fasting insulin and C-peptide levels in normal subjects (IRI 9.10 +/- 0.41 microU/ml; CPR 1.79 +/- 0.08 ng/ml), in obese subjects (IRI 11.31 +/- 0.38 microU/ml; CPR 2.54 +/- 0.07 ng/ml) in obese hypertensive subjects (IRI 14.17 +/- 0.72 microU/ml; CPR 2.64 +/- 0.09 ng/ml), in obese hypertensive diabetic subjects (IRI 22.57 +/- 2.62 microU/ml; CPR 3.33 +/- 0.27 ng/ml). Thus, we found increasing levels of IRI and CPR as normal conditions changed towards progressively more severe pathological conditions. Although several other factors contribute to determine CVD, we conclude that increasing levels of insulin and C-peptide could play an important role in causing CVD.

Erythrocyte glucose, ATP, lactate concentrations and their modifications induced by isologous plasma in non-insulin-dependent diabetes mellitus.

We determined erythrocyte glucose, ATP and lactate contents in diabetic subjects using an experimental design in which red blood cells (RBCs) were incubated over four hours in their own plasma and in plasma from normal subjects. The results indicated that baseline RBC glucose and lactate concentrations were higher in diabetic RBCs than in the controls, while ATP content was similar. After incubation, in diabetic RBCs glucose decreased significantly but more markedly when RBCs were incubated in normal plasma; lactate increased markedly in diabetic erythrocytes in their own plasma, but increased to the same extent as controls when incubated in normal plasma. ATP levels were similar to baseline values in diabetic RBCs in their own plasma, but decreased significantly when incubated in normal plasma. Since we found such a different metabolic behaviour in diabetic RBCs changing from diabetic to normal plasma, the important role of blood glucose in regulating RBC glycolysis is again confirmed.

[Plasma levels of beta-endorphin in obese subjects with normal glucose tolerance test and in diabetics]. / Livelli plasmatici di beta-endorfina in soggetti obesi normotolleranti e diabetici.

Forty obese subjects with normal glucose tolerance test (NGTT) thirteen diabetic obese subjects and sixteen normal subjects were studied to evaluate the possible interactions between beta-endorphin (B-Ep) and glucose homeostasis. On the basis of baseline B-Ep levels, two subgroups were selected: one group with normal mean values of B-Ep (7.02 +/- 0.59 pmol/l); another group with elevated mean values of B-Ep (18.95 +/- 1.52 pmol/l). No differences between these subgroups were found as regards body mass index (BMI), insulin and glucagon levels. Normal B-Ep values were found in diabetic obese subjects. No significant correlation was found between B-Ep and BMI, insulin or glucagon. Considering that B-Ep is involved in eating behavior and on the basis of our results, we suggest that elevated B-Ep levels can be found only in those obese NGTT subjects whose obesity is probably related to an abnormal modulation of food intake, such as hyperphagia.

Increase in red cell lactate concentration and its reduction by isologous plasma in NIDDM subjects.

We determined red blood cell (RBC) lactate concentrations in NIDDM subjects using an experimental protocol in which diabetic RBCs were incubated over 8 hours both with own plasma and with normal plasma. Furthermore, normal RBCs were incubated both with own plasma and with diabetic plasma. The results indicate that the increased lactate concentrations in RBCs from NIDDM subjects decreased significantly when the same RBCs were incubated in normal plasma. Conversely, lactate concentrations in normal RBCs increased significantly when RBCs were incubated in diabetic plasma. Thus, other than muscle and adipose tissue, RBCs may contribute to increase lactate release for hepatic gluconeogenesis in NIDDM and we suggest that there may be extrinsic plasmatic factor(s) capable of stimulatory effect on diabetic RBC glycolytic pathway.