1. Diene-conjugated fatty acids are one of the products of free-radical attack upon lipids and therefore have been used as markers of such attack. The major diene-conjugated fatty acid in human tissue and serum is an isomer of linoleic acid (9,12-octadecadienoic acid), namely 9,11-octadecadienoic acid. Diet may be another source of this isomer, raising questions as to its value as a free-radical marker. The aim of this study was to determine the importance of diet as a source of 9,11-octadecadienoic acid in phospholipid esterified fatty acids in human serum. 2. Foodstuffs rich in 9,11-octadecadienoic acid were identified. Fourteen subjects volunteered to alter their diets, either increasing ('high diet') or decreasing ('low diet') their intake of these foodstuffs for 3 weeks. Where subjects undertook both diets, a washout period of at least 3 weeks was allowed between phases. 3. Seven-day diet histories were kept and scored with respect to their content of 9,11-octadecadienoic acid. The concentrations of 9,11-octadecadienoic acid and linoleic acid in serum phospholipids were measured by h.p.l.c. with u.v. detection. 4. The percentage molar ratio of 9,11-octadecadienoic acid to linoleic acid was calculated. The percentage molar ratio rose significantly on the 'high diet' [1.3(0.4) versus 1.9(0.7), P = 0.01, mean (SD)] and fell significantly on the 'low diet' [1.6(0.4) versus 1.1(0.4), P = 0.004, means (SD)]. There was a significant correlation between the change in dietary intake of 9,11-octadecadienoic acid and the change in the percentage molar ratio (r = 0.829, P = 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
The aim of this study was to evaluate the effects of a fish oil preparation (MaxEPA) on hemostatic function and fasting lipid and glucose levels in non-insulin-dependent diabetic (NIDDM) subjects. Eighty NIDDM outpatients aged 55.9 yr (mean SD 11.5 yr) participated in a prospective double-blind placebo-controlled study of MaxEPA capsules (10 g/day) or olive oil (control) treatment over 6 wk. Patients received either MaxEPA or olive oil in addition to preexisting therapy. Metabolic and hemostatic variables were measured before treatment and after 3 and 6 wk. Platelet membrane eicosapentaenoic acid (EPA) content increased in the treatment group (P less than 0.001). MaxEPA supplementation was associated with a significant fall in total triglycerides (P less than 0.001) but did not affect total cholesterol (P = 0.7) compared with control treatment. Fasting plasma glucose increased after 3 wk (P = 0.01) but not after 6 wk (P = 0.17) treatment with MaxEPA. Spontaneous platelet aggregation in whole blood fell in the MaxEPA group (P less than 0.02) after 6 wk, but there were no changes in agonist-induced platelet aggregation, thromboxane generation in platelet-rich plasma, or plasma beta-thromboglobulin and platelet factor IV levels. An increase in clotting factor VII (P = 0.02), without changes in fibrinogen or factor X levels, occurred in the MaxEPA group. Similar reductions in blood pressure were observed in both groups. Dietary supplementation with MaxEPA capsules (10 g/day) in NIDDM subjects is associated with improvement in hypertriglyceridemia but with deleterious effects in factor VII and blood glucose levels. Most indices of platelet function are unaffected by this therapy.
The prevalence of diabetes in the elderly is high. Hypoglycaemia is a treatment-related complication of diabetes. Owing to age-related changes, decreased perception of hypoglycaemic symptoms, comorbidities and polypharmacy, elderly diabetic persons are at a greater risk of developing hypoglycaemia. Other risk factors include longer duration of diabetes, history of previous hypoglycaemic episodes, intensive glycaemic control, poor nutrition or missed meals and recent hospitalisation. Insulin and sulphonylureas are the medication classes most frequently associated with hypoglycaemia. Other antidiabetic medications typically cause hypoglycaemia only when used in combination with sulphonylureas or insulin. Hypoglycaemia in older people is associated with loss of independence, increased morbidity and mortality. Prevention of hypoglycaemia requires recognition of the risk, identification of precipitating factors, patient and caregiver education, appropriate prescribing and ongoing health professional support.
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