Oral Glucose Tolerance and Related Factors in a Normal Population Sample--I. Blood Sugar, Plasma Insulin, Glyceride, and Cholesterol Measurements and the Effects of Age and Sex

Boyns, D. R.; Crossley, J. N.; Abrams, M. E.; Jarrett, R. J.; Keen, H.

doi:10.1136/bmj.1.5644.595

Cited by 98 publications

(32 citation statements)

References 13 publications

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“…Finally, the report of an increasing serum estradiol and decreasing serum testosterone concentration with aging in men (32) is consistent with the increasing incidence of myocardial infarction observed with aging (33) and may also explain at least in part the decreasing glucose tolerance (34) with increasing insulin response (35), increasing serum cholesterol and triglyceride concentrations (34), increasing blood pressure (36), impotence, tendency to obesity (37), and perhaps other concomitants of aging as well. …”

Section: Discussionsupporting

confidence: 67%

Relationship between serum sex hormones and glucose, insulin and lipid abnormalities in men with myocardial infarction.

Phillips¹

1977

Proc. Natl. Acad. Sci. U.S.A.

106

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Fifteen patients who had had a myocardial infarction before the age of 43 were compared with thirteen age-matched normal subjects. Twelve of the patients and three of the controls had a delayed glucose and insulin peak in the glucose tolerance test. Curves with delayed peaks defin larger mean glucose and insulin areas than normal curves. When the measurements of the four patients with the largest areas under the glucose tolerance curve were separated, significant correlations were observed in the remaining patients and controls.The ratio in serum of the concentrations of estradiol-17j# to testosterone (E/) correlated with serum glucose area (r = +0.69, P < 0.001), insulin area (r = +0.80, P < 0.001), and the ratio of insulin area to glucose area (I/G) (r = +0.64, P < 0.005) in the glucose tolerance test. Serum cholesterol concentration correlated with E/T, insulin area, and I/G, and serum triglyceride concentration correlated with glucose area, I/G, and serum cholesterol concentration. The hypothesis is presented (i) that in men who have had a myocardial infarction, an abnormality in glucose tolerance and insulin response and elevation in serum cholesterol and triglyceride concentrations are all part of the same defect (glucose-insulin-lipid defect), (ii) that this glucose-insulin-lipid defect when glucose intolerance is present is the "mild diabetes" commonly associated with myocardial infarction but is based on a mechanism different from that of classical diabetes, (iii) that this glucose-insulin-lipid defect is secondary to an elevation in E/T, and (iv) that an alteration in the sex hormone milieu is the major predisposing factor for myocardial infarction.An abnormality in glucose tolerance, insulin response, serum lipid or lipoprotein concentrations, or some combination of these has been reported to occur in 80-96% of patients with coronary heart disease (1-7). In a previous study (8), a high incidence of hyperestrogenemia was observed in men under 44 years of age with myocardial infarction. The present report describes further investigations carried out on the patients and normal subjects of that study in order to determine whether the hyperestrogenemia was related to the glucose, insulin, and lipid abnormalities. The results of these investigations show a high level of correlation between the degrees of the glucose and insulin defects and the ratio of the weight concentrations in serum of estradiol-17fl to testosterone (E/T). The degree of the glucose-insulin defect was also found to correlate with the serum cholesterol and triglyceride concentrations, suggesting that an elevation in the concentrations of these lipids is part of the same defect (glucose-insulin-lipid defect). These observations raise the possibility that this glucose-insulin-lipid defect is secondary to an elevation in E/T and that a disturbance in the relationships of serum sex hormones is the major predisposing factor for myocardial infarction in men.

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Section: Discussionsupporting

confidence: 67%

Relationship between serum sex hormones and glucose, insulin and lipid abnormalities in men with myocardial infarction.

Phillips¹

1977

Proc. Natl. Acad. Sci. U.S.A.

106

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“…Although women have a lower skeletal muscle mass than men, a review of the literature points to improved glucose tolerance and heightened skeletal muscle insulin sensitivity in normal women compared with men (11)(12)(13). Thus, Fernandez-Real et al (14) have shown that premenopausal women are more insulin sensitive than men when the groups are matched for body fat, and Yki-Jarvinen (13) has shown enhanced insulin sensitivity in women versus men when insulin-stimulated glucose disposal is expressed as a function of muscle mass.…”

mentioning

confidence: 99%

Female Rats Do Not Exhibit Free Fatty Acid–Induced Insulin Resistance

Hevener

Reichart²,

Janež³

et al. 2002

Diabetes

101

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It is well described that excessive lipid metabolism can cause insulin resistance in both animals and humans, and this has been implicated as a causative factor in the development of insulin resistance and type 2 diabetes in humans. Recently, we have shown that intravenous lipid emulsion (liposyn) infusion during a 120-min euglycemichyperinsulinemic clamp led to significant reductions in insulin action and fatty acid translocase (FAT/CD36) skeletal muscle protein expression. After reviewing the literature, it became evident that essentially all past studies, including our own, were conducted in male animals. Therefore, to determine whether there were sex determinants of fat-induced insulin resistance, we assessed the impact of free fatty acid (FFA) elevation on insulin action in female rats. Here, we report that a fourfold elevation in plasma FFA concentration induced a 40% reduction in the insulin-stimulated glucose disposal rate, a 30% decline in insulin-stimulated skeletal muscle insulin substrate receptor-1 (IRS-1) phosphorylation, a 48% decrease in IRS-1-associated phosphatidylinositol (PI) 3-kinase activity, and a 50% reduction in muscle FAT/CD36 protein expression in male rats. In striking contrast, we found no effect of FFA elevation to cause insulin resistance, changes in IRS-1/PI 3-kinase, or FAT/CD36 protein levels in female animals. Our findings indicate that female animals are protected from lipid-induced reductions in insulin action. Diabetes 51: [1907][1908][1909][1910][1911][1912] 2002 I t is widely held that excessive lipid metabolism, achieved either by high-fat feeding or intravenous infusion of lipid emulsion to raise circulating free fatty acid (FFA) levels, leads to decreased insulinstimulated glucose uptake (1-10). This lipid-induced decrease in insulin-stimulated glucose disposal is associated with a decline in insulin substrate receptor-1 (IRS-1)-associated phosphatidylinositol (PI) 3-kinase activity in skeletal muscle, and these in vivo and in vitro findings have been reported in several articles (1,6,9,10) and are well supported. Interestingly, after reviewing the literature, it became apparent that essentially all studies reporting fat-induced insulin resistance in humans or rodents have been conducted in men or male animals. Because the prevailing concept is that fat-induced impairment of glucose disposal is a major risk factor for the development of insulin resistance and type 2 diabetes, and because type 2 diabetes is equally prevalent in men and women, it is important to determine whether the deleterious effects of increased fat metabolism are the same for males and females.Although women have a lower skeletal muscle mass than men, a review of the literature points to improved glucose tolerance and heightened skeletal muscle insulin sensitivity in normal women compared with men (11-13). Thus, Fernandez-Real et al. (14) have shown that premenopausal women are more insulin sensitive than men when the groups are matched for body fat, and Yki-Jarvinen (13) has shown enhanced insuli...

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“…In a study which antedated the current interest in HDL cholesterol [3,4], we found that in men, but not in women, fasting plasma insulin levels were negatively correlated with total calorie intake. Although body mass index was the strongest correlate of plasma insulin, the insulin/diet relationship was statistically independent of this [4].…”

Section: Hdl Cholesterol and Fasting Insulin Levelsmentioning

confidence: 95%