PubMed · 6404166
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S A Blumenthal. 1983. Sulfonylureas and platelet function.. https://doi.org/10.1016/0002-9343(83)91067-7
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Associations between loss of glucose tolerance, insulin resistance, and ischemic heart disease (IHD) are of great current concern. Considerable controversy and uncertainty relates to the mechanism(s) that underlies these associations. Whilst there is some evidence in prospective studies of an association between hyperinsulinemia and future IHD, it is by no means strong or consistent between different studies. Hypertriglyceridemia is another possible factor involved in the linkage between glucose intolerance and IHD. There is good evidence for an affect of plasma nonesterified fatty acids (NEFA) to increase hepatic output of VLDL. Insulin, contrary to some suggestions, acts to lower plasma VLDL by actions directly on hepatic output and activation of adipose tissue lipoprotein lipase, and indirectly via the hormones affect of lowering plasma NEFA. Glycosylation and oxidation of lipoproteins may enhance their atherogenic potential. It is highly probable that procoagulant changes are also important processes predisposing to IHD. Associations between plasminogen activator inhibitor-1 and insulin, intact and 32,33 split proinsulin hypertriglyceridemia, and insulin resistance have been reported, but a unifying hypothesis explaining these links remains elusive. Epidemiological studies now repeated in a number of centers have shown links between infant mortality and birth weight and risk of IHD, and between birth weight and risk of impaired glucose tolerance and non-insulin-dependent diabetes mellitus (NIDDM). It has been proposed, therefore, that impairment of fetal and infant growth may underlie the associations between loss of glucose tolerance and risk of IHD. Animal models form the basis of much current research to test this concept.
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Changes in leg skin temperature during and after cigarette smoking were examined in 25 diabetics with autonomic neuropathy (au-neuropathy) (mean age 52 +/- 2 years) and 23 without (mean age 49 +/- 2 years), and 15 normal controls (mean age 49 +/- 2 years) using a Thermoviewer JTG 3300. All subjects were habitual smokers. Japanese Seven Star cigarettes (each containing 1.2 mg nicotine) were used for the test. Tender brand cigarettes (0.3 mg) were used additionally to compare the effect of nicotine content on the results. The smoking-stimulated thermographic pattern in the control group was rather flat, with a slight decrease in temperature followed by a slight increase before returning to the baseline level 15-20 min after smoking. The frequency of the typical temperature decreasing pattern, characterized by a profound decrease and gradual return to the baseline level in about 1 h, was significantly higher in the diabetic group than in the control group (33/48 vs 1/15; P less than 0.005). A comparison of the two diabetic subgroups revealed that the frequency was considerably higher in the subgroup with au-neuropathy (23/25 vs 10/23). These results suggest that au-neuropathy affects smoking-induced vasoconstriction in diabetic subjects. The maximum temperature decreases recorded were 1.5 +/- 2.0 and 2.69 +/- 0.24 degrees C in the controls and diabetics with au-neuropathy, respectively. The effect of Tender cigarettes with a low nicotine content was much weaker than that of Seven Star, which further suggests that smoking-induced vasoconstriction was also nicotine-dependent.