[Diet therapy in non-insulin dependent diabetes mellitus (NIDDM)]. / La dieta nel diabete di tipo II.

The main approach in NIDDM therapy is diet. Most patients present insulin resistance characterized by overweight, VLDL increase, minimal increase of LDL, decrease of HDL cholesterol, and hypertension. The overall goals of nutrition therapy are the maintenance of near normal glucose levels, and the achievement of optimal serum lipid levels with adequate calories for maintaining or attaining a reasonable body weight. In presence of obesity and hypertension even a slightly weight loss could achieve an improvement in metabolic control and in hypertension with a better life expectance. General-ly carbohydrate intake would represent the 50-60% of total caloric amount (with preference to those with low glycemic index), and lipids no more than 35% (less than 10% of these 10-15% from monounsaturated fats with less than 300 mg/day of cholesterol). If elevated very low density lipoproteins level is the primary problem, a beneficial approach is 10% of total caloric intake from saturated fats, 10% from polyunsaturated, and 15-20% from monounsaturated fats with less than 200 mg/day of cholesterol and 40% of carbohydrates. A large amount of fructose (20% of calories) may increase LDL levels but sweeteners as saccarine or aspartame are approved and determine a better diet compliance. Daily consumpion of 20-35 g of dietary fibres from food sources is recommended for metabolic control. Protein intake would be of about 10% of total caloric amount especially in presence of diabetic nepropathy. Alcohol would not exceed 30 g/day for men and 20 g/day for women keeping in mild that alcohol may worsen metabolic control, diet compliance, and may be dangerous itself. For people with hypertension a decrease of dietary sodium intake is recommended. Nutritional recommendations are developed to meet treatment goals and desired outcomes. Monitoring metabolic parameters, blood pressure, and body weight is very important to ensure successful outcomes.

Postprandial triglyceride-rich lipoprotein changes in elderly and young subjects.

To determine whether an increased risk for atherosclerosis in older humans is related to changes in postprandial lipoprotein metabolism, we compared the dynamic profiles (0-10 hours) of triglyceride (Tg)-rich lipoproteins and the Tg content in VLDL subfractions in elderly and young subjects after an oral fat load. The plasma Tg response curves displayed significant differences between the groups at all times. Postprandial triglyceridemia was quantified from the plasma response curves as an incremental area, and was significantly different in the two groups (young subjects 231.9 +/- 199.6 vs elderly subjects 511.0 +/- 305.6 mg/dL x 10 hr, p = 0.036). The more scattered VLDL-Tg values were significantly different compared to values at baseline and 6 hours after fat load. Tg baselines in the four VLDL subfractions (expressed as percentages) were higher in the larger particles (B Sf = 175-400) in the elderly subjects, and in the smaller, denser particles (D Sf = 20-100) in the young subjects. In both groups, postprandial hyperlipidemia increased the Tg content of the larger, less dense particles (Sf more than 400), and reduced that of the denser particles. These variations usually coincided with the plasma Tg and VLDL peaks: 63% to 70% above the Tg baseline between the 2nd and 4th hour in all the young subjects: 48% to 68% above the baseline between the 4th and the 6th hour in all the elderly subjects. Total cholesterol variations showed no significant differences between the two groups at any time. All subjects tested for the missense mutation at codon 188 of the human lipoprotein lipase (LPL) gene resulted noncarriers of LPL mutant alleles. Our data show that, after a fatty meal, healthy elderly subjects tend to present prolonged postprandial hypertriglyceridemia, suggesting an atherogenic behavior of their lipid metabolism.

Insulin resistance shows selective metabolic and hormonal targets in the elderly.

There has been no simultaneous evaluation of different aspects of insulin action in ageing. We studied 12 elderly (77 +/- 2 years) and 12 young (26 +/- 1 years) subjects with normal glucose tolerance and matched for sex, body mass index, lean body mass (LBM), blood pressure and physical activity, using a euglycaemic-hyperinsulinaemic clamp at about 350 pmol L-1 in combination with [3H]-glucose infusion. In the elderly group, hepatic glucose production was normal, fasting serum insulin and C-peptide were significantly increased (P = 0.001) and glucose utilization (34.4 +/- 2.4 vs. 44.4 +/- 3.2 mumol kg-1 LBM min-1, P = 0.02) and the percentage maximal suppression of C-peptide (58 +/- 6% vs. 79 +/- 5%, P = 0.02) during the clamp were reduced. Fasting plasma free fatty acid (FFA) and glycerol levels were similar in the two groups, but their percentage maximal suppression during the clamp was reduced in the elderly group (FFA 45 +/- 5% vs. 77 +/- 6%, P = 0.001; glycerol 43 +/- 5% vs. 76 +/- 3%, P = 0.001). Branched-chain amino acids (valine, leucine, isoleucine) and glucagon levels were similar in the two groups, both while fasting and during the clamp. Thus, insulin resistance in ageing appears selective on glucose utilization, inhibition of lipolysis and feedback inhibition of the B-cell secretion.