OBJECTIVE - To determine whether the severity of retinopathy is higher in a group of NIDDM patients with sBP greater-than-or-equal-to 140 mmHg compared with NIDDM patients with sBP < 140 mmHg.RESEARCH DESIGN AND METHODS - Ophthalmoscopy and FAG were conducted among a group of NIDDM patients with either a sBP above (n = 54) or below (n = 55) 140 mmHg. The groups were matched according to diabetes duration, metabolic control (HbA1c), and AER.RESULTS - Patients with sBP > 140 mmHg had a higher prevalence of retinopathy, as established according to a rating scale (4.9 +/- 3.8 vs. 3.2 +/- 3.3, P < 0.02); furthermore, their BMI values were higher (28.1 +/- 4.5 vs. 24.9 +/- 4.1 kg/m2, P < 0.001). The group of normotensive subjects showed the highest rate of low grading (0-2) values. However, the highest prevalence rates of 8-10 grading values (proliferative retinopathy) were found in the hypertensive group.CONCLUSIONS - These data suggest that sBP values greater-than-or-equal-to 140 mmHg favor the onset of retinopathy in NIDDM patients during their 1st 10 yr of disease.

The influence of plasma lipid disorders on red blood cell (RBC) lipid pattern and some related erythrocyte membrane functions, such as glycerol (GLT50) permeability and erythrocyte deformability was studied in diabetes mellitus. Significantly higher red blood cell cholesterol content, GLT50 and erythrocyte filtration time values were found in diabetics. GLT50 values were found closely related to both RBC cholesterol content (r = 0.84, p less than 0.001) and filtration time (r = 0.60, p less than 0.001). Interestingly, six diabetics with retinopathy showed GLT50 values above 60 sec. The RBC Cholesterol/Phospholipids molar ratio was significantly higher in diabetics. The most notable changes of plasma lipid pattern in diabetics were a decrease of both plasma HDL cholesterol, phospholipids and Apolipoprotein A levels with an increase of HDL free cholesterol/phospholipids molar ratio. RBC cholesterol content was found to be inversely related to HDL esterified/free cholesterol molar ratio (r = -0.56, p less than 0.001), while RBC cholesterol/phospholipids molar ratio was significantly related to both HDL free cholesterol/phospholipids (r = 0.51, p. 0.001) and to LDL total cholesterol/phospholipids (r = 0.25, p less than 0.05). Lastly, HDL cholesterol levels were found to inversely relate to glycosylated haemoglobin values (r = -0.54, p less than 0.01).

The study was designed to determine eventual correlation in diabetes mellitus between reduced erythrocyte deformability and red blood cells (RBC) cholesterol content. Significantly higher RBC cholesterol amount was found in 11 diabetics (IDDM) than in 13 controls of similar age (45 +/- 10 yrs) (1.30 mg ml-1 packed cells -1 +/- 0.15 SD vs 1.19 +/- 0.10 SD, p less than 0.05). Blood filterability values have been found significantly higher (p less than 0.025) in the diabetics (42.2 +/- 11.5 SD ml sec. -1) than in controls (33.5 +/- 6.0). Flow time of RBC filterability, measured in erythrocyte saline buffered suspension (40% Hct) in order to eliminate interferences from plasmatic factors, showed a closely correlation with RBC cholesterol content (r = 0.86 p less than 0.01). A significant inverse correlation between RBC cholesterol content and serum ApoA1-HDL levels was also observed (r = -0.58, p less than 0.05). Moreover ApoA1-HDL serum values were significantly (P less than 0.01) lower in diabetics (111.8 +/- 10.1 mg/dl) than in controls (126 +/- 6.6 mg/dl). Our data underline the possible involvement of augmented erythrocyte cholesterol in impairing the microhemologic competence of RBC in diabetes mellitus. A possible relation with lower ApoA1-HDL and lecithin-cholesterol-acyl-transferase (LCAT) is examined.

Pyruvate-dehydrogenase, an enzymatic mitochondrial complex, exists in both inactive and active forms, insulin being the regulating factor of the transformation of a latter into the former. The basal (PDHb) and total (PDHt) activity of this enzyme in adipose tissue mitochondria from obese hyperinsulinemic humans has been found equal to 1014 +/- 459 SD mU respectively. These values are 250% higher than those found in normal subjects (403 +/- 76 SD and 575 +/- 142 SD respectively). Both in normal and obese subjects the PDHb/PDHt percent ratio was equal to about 70. These results show that insulin, undoubtedly hyperactive in obesity, by activating PDH can induce a major synthesis of fat, a high caloric density tissue.