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Fasting blood glucose and serum immunoreactive insulin (IRI) and the responses of blood glucose and serum IRI to peroral glucose challenge were investigated in middle-aged normoglycemic male twins of 17 monozygotic (MZ) and 18 dizygotic (DZ) pairs recruited from the Finnish Twin Cohort Study. Also, the role of obesity and diet in the regulation of glucose and insulin metabolism was estimated. The fasting and 2 hr postprandial (PP) glucose showed higher pairwise correlations in MZ (r =0.78 and 0.56) than DZ (r = 0.08 and −0.05) pairs whereas fasting and PP insulin levels and the areas under the PP glucose and insulin curves were weakly and similarly correlated in MZ and DZ twins. The pairwise correlations of the 1/2 hr and 1 hr, but not the fasting and 2 hr insulin/glucose ratios, were somewhat higher in MZ (R = 0.51 and 0.53) than DZ (r = = 0.28 and 0.30) pairs. In MZ twins, the intrapair differences in the body mass index were significantly correlated with those in the fasting and 2 hr PP glucose and insulin levels and those in the fasting and 1/2 hr insulin/glucose ratios (r from 0.47 to 0.76). Also, the intrapair differences in the dietary fat calories were correlated positively, but those in the calories derived from carbohydrates negatively, with the intrapair differences in several parameters of the glucose and insulin metabolism. These data suggest that the environmental contribution to the regulation of glucose and insulin metabolism in subjects within the normoglycemic range may be quite strong. Of the environmental factors studied, obesity and dietary fat consumption seem to have powerful regulatory roles, particularly in the response of insulin to the glucose load.

Fatty acid patterns of plasma and platelet lipids, platelet aggregation and thromboxane A2(TxA2) production were studied in young patients (n = 12) with brain infarction and in healthy controls (n = 13). Platelet arachidonic acid content was significantly reduced in the stroke patients, but in vitro platelet aggregation was similar in the two groups. A low dose of acetosalicylic acid (ASA) (100 mg) suppressed thromboxane production and normalized the platelet arachidonic acid values. The low arachidonic acid in platelets is probably due to its increased consumption, indicating platelet activation in vivo.

Urinary excretion of neuraminyl lactose and neuraminyl N-acetyllactosamine was studied in 22 subjects with suspected myocardial infarction. The excretion was increased in all patients with verified infarction, whereas only a negligible change was seen in three subjects with angina pectoris without signs of myocardial damage. High levels of excretion were seen in patients with large infarctions, whereas relatively small changes were found in two patients with subendocardial infarction. Maximal excretion of neuraminyl lactose was attained 3 to 4 days after the onset of pain the peak occurring slightly later than the maximum serum aspartate aminotransferase, but preceding the respective peaks of erythrocyte sedimentation rate and serum total neuraminic acid. Urinary excretion of high molecular weight neuraminic acid-containing compounds was also increased in patients with myocardial infarction, the peak almost coinciding with the maximum of neuraminyl lactose excretion. No consistent changes were seen in the urinary output of lactose of free neuraminic acid. Neuraminic acid content of myocardium, although increased in the infarcted area, was so low that direct release of neuraminic acid-containing material from necrotic tissue could not explain the increase in urinary neuraminyl oligosaccharides after myocardial infarction. It is suggested that increased urinary excretion of neuraminic acid-containing compounds is derived from some extramyocardial tissue, possibly from the liver.

A comparative study has been made of the action of 3-methyl salicylic acid, a derivative which has a much longer half-life than salicylic acid in man, on free fatty acid mobilisation and plasma cholesterol in the rat, rabbit, baboon and man. 3-Methyl salicylic acid decreased plasma free fatty acids in rats exposed to conditions of increased mobilisation, such as fasting, cold, and treatment with noradrenaline and ACTH. Evidence was obtained that a dose equivalent to salicylic acid given shortly before test was more effective. As for salicylate, 3-methyl salicylate decreased the in vitro production of FFA and glycerol liberated in vitro by the incubated rat epididymal fat pad. Administration of 3-methyl salicylic acid (100 mg/kg, body weight) reduced plasma cholesterol from 7 to 45% in baboons given an atherogenic, cholesterol-containing diet for one month. In acute experiments, the drug caused a marked choleresis in which the volume and excretion of bile acids but not cholesterol was increased. In the rabbit, the drug (100 mg/kg) caused a decrease in fasting FFA for up to four hours, followed by a large elevation. Inclusion of the drug in the diet of animals given a semi-synthetic diet of low cholesterol content did not reduce hypercholesterolaemia or the extent and severity of atherosclerotic lesions in the aorta. Administration of 0.9 g orally to fasting patients caused a 50% reduction in elevated plasma FFA after four hours and even after twelve hours the values were still subnormal. A double-blind control trial of nine hypercholesterolaemic and eight normal patients was conducted over twelve to eighteen months. Subjects in the hypercholesterolaemic group on chronic dosage (0.9–1.8 g per day) showed a fall of 25% in the mean plasma cholesterol, but there was no change in normal patients. Side effects, the chief of which were drowsiness and vomiting precluded the use of 3-methyl salicylate as a therapeutic agent in man.

Clofibrate treatment decreased drastically the activity of serum postheparin lipoprotein lipase of rats fed with fat-free test diet but had no effect on hepatic lipase. 3 weeks' treatment was followed by a significant fall in serum cholesterol caused by a marked decrease in HDL-cholesterol. Clofibrate decreased in vitro synthesis of cholesterol and fatty acids in jejunal villous cells but not in the crypt cells.