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Biomedical subjects

S G Mendoza

Publications and source records attributed to S G Mendoza.

10 recordsLinked to original sources
PubMed1997

Metformin therapy is associated with a decrease in plasma plasminogen activator inhibitor-1, lipoprotein(a), and immunoreactive insulin levels in patients with the polycystic ovary syndrome.

Sixteen nondiabetic women with polycystic ovary syndrome (PCOS) aged 18 to 33 years were studied before and after 8 weeks on metformin (1.5 g/d) therapy to assess whether reducing hyperinsulinemia would reduce the levels of the major inhibitor of fibrinolysis, antigenic plasminogen activator inhibitor type 1 (PAI-1). Compared with six normal control women, PCOS women had a higher body mass index (BMI), waist to hip ratio, fasting insulin (Izero), insulin area under the curve during oral glucose tolerance testing (IA), glucose area under the curve during oral glucose tolerance testing (GA), IA/GA ratio, PAI-1, luteinizing hormone (LH) and ratio of LH to follicle-stimulating hormone (FSH), and free testosterone, and lower high-density lipoprotein (HDL) cholesterol (all P < .025). On metformin, BMI decreased 1.3% (P = .04), Izero 43% (P = .002), IA 31% (P = .03), GA 11% (P = .02), PAI-1 16% (P = .01), lipoprotein(a) [Lp(a)] 42% (P = .004), free testosterone 46% (P = .0006), LH 44% (P = .004), and the LH/FSH ratio 41% (P = .0001). On metformin, absolute and percent reductions in Izero correlated with absolute and percent reductions in PAI-1 (r = .60, P = .015 and r = .64, P = .008). On metformin, by stepwise multiple regression, the absolute reduction in Izero was a significant determinant of the absolute reduction in PAI-1 (partial R2 = 35%, P = .02), and the percent reduction in Izero was a significant determinant of the percent reduction in PAI-1 (partial R2 = 52%, P = .003). Metformin decreases Izero in hyperinsulinemic PCOS patients, reverses the hyperinsulinemia-driven endocrinopathy, decreases PAI-1, and decreases Lp(a), and should thus reduce the increased risk of atherothrombosis in PCOS.

Adolescent↗
PubMed1997

Menstrual cyclicity after metformin therapy in polycystic ovary syndrome.

OBJECTIVE: To assess the effect of insulin-lowering treatment on menstrual cyclicity in polycystic ovary syndrome (PCOS). METHODS: Forty oligoamenorrheic women with PCOS were recruited in a prospective clinical study to receive metformin for a minimum period of 6 months. Twenty-two women completed the study. Serum LH, FSH, free testosterone, and glucose and insulin response to oral glucose load were measured both before and after 8 weeks of metformin treatment. Menstrual cyclicity and serum progesterone levels at the midluteal phase were assessed at the 30th week of metformin treatment. RESULTS: Twenty-one of 22 women had restoration of menstrual cyclicity (95.7%). Four of these women (19%) became pregnant within the 6th and 7th months of treatment. All four of the pregnant women delivered, and the infants were healthy. Thirteen of 15 women who had regular menses demonstrated a serum progesterone level within the ovulatory range (3.1-28 ng/mL). Fasting (P < .001) and the integrated insulin response to the glucose load decreased (P < .001) after 8 weeks of metformin treatment. This was accompanied by significant decreases in serum LH (P < .001) and free testosterone (P < .001) levels and LH/FSH ratio (P < .001). There was a small but significant reduction in body mass index after 8 weeks of metformin treatment (P < .001). CONCLUSION: A 6-month course of metformin may improve menstrual cyclicity and fertility in women with the PCOS. Insulin-sensitizing agents provide a rational approach to the treatment of the metabolic and endocrine abnormalities in PCOS women.

Adult↗
PubMed1991

Effect of physical training on lipids, lipoproteins, apolipoproteins, lipases, and endogenous sex hormones in men with premature myocardial infarction.

In 17 men, aged 27 to 54 years, with myocardial infarction 2 to 10 months before the current exercise study, we aimed to determine whether 3 months of exercise training, at a level designed to elevate high-density lipoprotein cholesterol (HDLC), would be associated with changes in endogenous sex steroid hormones and postheparin lipoprotein and hepatic lipases, and whether the changes in sex hormones, lipids, lipoproteins, apolipoproteins, and physical activity were interrelated. Supervised bicycle ergometry, 30 minutes, 3 days per week, eliciting 75% of maximum heart rate, produced a significant training effect, with a 26% increase in the duration of the exercise test at a standardized, submaximal workload (P less than or equal to .001), and a reduction in heart rate measured at a standardized submaximal workload, P = .08. After 3 months' training, mean HDLC increased 23% (30 to 37 mg/dL), P less than or equal to .001, mean apo A2 increased 19% (43 to 51 mg/dL), P less than or equal to .001, and the ratio of total cholesterol (TC) to HDLC decreased 26% (P less than or equal to .01), while estradiol (E2) levels decreased 45% (50.1 to 27.8 pg/mL), P less than or equal to .0001. After 1 and 2 months' exercise, TC (12% [P less than or equal to .001], 11% [P less than or equal to .01]), and low-density lipoprotein cholesterol (LDLC) (13% [P less than or equal to .01], 12% [P less than or equal to .01]) were reduced. Hepatic lipase decreased 16% (P less than or equal to .01) and 16% (P less than or equal to .05) after 1 and 3 months' exercise. There were no significant changes in apo A1, lipoprotein lipase, testosterone, luteinizing hormone (LH), follicle-stimulating hormone (FSH), or weight. By stepwise regression analysis, after 3 months' training, 66% (P = .0025) of the variance for the increase in HDLC from baseline to day 90 was accounted for independently by a decrease in triglyceride (F = 13.2, P = .003), by reduced heart rate on a fixed submaximal load (F = 12.7, P = .0035), and by a decrease in hepatic lipase (F = 5.5, P = .036). A modest, achievable exercise program can have significant cardiovascular benefit for men after myocardial infarction by ameliorating their hyperestrogenemia, reducing TC and LDLC, improving the TC to HDLC ratio, and elevating HDLC and apo A2. The increment in HDLC was related independently to improved capacity to sustain submaximal exercise and to exercise-induced reductions in triglyceride and postheparin hepatic lipase.

Adult↗
PubMed1990

Effect of ketoconazole on plasma sex hormones, lipids, lipoproteins, and apolipoproteins in hyperandrogenic women.

The aim of the current study of 18 hyperandrogenic women was to determine the affects of ketoconazole (KTZ), an oral synthetic antifungal imidazole derivative that inhibits gonadal and adrenal steroidogenesis, on lipids, lipoprotein cholesterols, apolipoproteins, endogenous sex steroid hormones, and their interactions. Eighteen hyperandrogenic women, ages 18 to 35, with a history of severe acne and/or hirsutism, were randomly divided into two groups of nine, both receiving KTZ (group 1, 400 mg/d; group 2,800 mg/d) for 10 days. In groups 1 and 2, KTZ therapy reduced cholesterol (10%, P less than or equal to .01; 19%, P less than or equal to .05) and low-density lipoprotein (LDL)-cholesterol (13%, P less than or equal to .05; 33%, P less than or equal to .025), and increased apolipoprotein (apo) A1 (7%, P less than or equal to .005; 13%, P less than or equal to .01). KTZ, 800 mg/d, decreased apo B (21%, P less than or equal to .005), and lowered the ratio of LDL-cholesterol to high-density lipoprotein (HDL)-cholesterol (40%, P less than or equal to .01). KTZ therapy more than doubled the levels of estradiol (E2) in both groups (136%, P less than or equal to .01; 171%, P less than or equal to .01) and, in the high-dose group, decreased the levels of free testosterone (FT) (48%, P less than or equal to .05) and dehydroepiandrosterone-sulfate (DHEA-S) (36%, P less than or equal to .005). The reductions of total and LDL-cholesterol appear to be attributable to the increases in E2 and possibly to the decrease in FT. KTZ therapy may have beneficial effects on atherogenic lipid and lipoprotein patterns in women with hyperandrogenicity.

Adolescent↗
PubMed1988

High-density lipoprotein apolipoprotein AI and AII turnover in moderate and severe proteinuria.

The kinetic parameters of high-density lipoprotein (HDL) and its major apolipoproteins (Apo) AI and Apo AII were studied in 2 patients with moderate and severe proteinuria and 2 normal controls after intravenous injection of autologous 125I-HDL. The fractional catabolic rates (FCR) of HDL estimated by urine/plasma radioactivity ratio, and FCR of Apo AI and Apo AII calculated from the radioactivity decay curves were higher in the patients. These results support the concept that high-density lipoproteinuria and renal parenchymal sequestration of HDL found in the nephrotic syndrome contribute to accelerated HDL catabolism.

Adult↗
PubMed1986

Sex hormones, lipids, lipoprotein cholesterols, and apolipoproteins in normal and obese subjects: atherogenic relationships.

Our aim in the current study of 20 normal controls, 28 overweight, and 26 severely overweight (obese) subjects was to assess interrelationships of obesity, endogenous estradiol (E2) and testosterone (T), and the E2/T ratio with major independent explanatory variables for coronary heart disease (CHD), including lipids, lipoproteins, and apolipoproteins. Most of the lipid and lipoprotein variables (total, high-, low-, and very-low-density lipoprotein cholesterols) as well as apolipoproteins A1, A2, and B did not vary significantly with the presence of obesity. With increasing relative ponderosity, there were, however, increasing levels of total triglycerides and VLDL triglyceride. Levels of FSH, LH, prolactin, and testosterone did not differ significantly with obesity. The obese subjects had the highest E2 and E2/T levels; overweight subjects had intermediate levels which were also significantly higher than in the controls. Using multiple regression analyses, in obese subjects increasing T was associated with increasing apo B, and increasing E2 was correlated with decreasing apo A1. Opposite relationships were found in the normal controls where increasing T and increasing Quetelet indices were associated with diminished apo B and increasing E2 was associated with increasing A1. Obesity's association with increased CHD risk may be mediated through increasing E2 and apo B and reducing apo A1. Since obese subjects have higher E2 levels and often have lower T, they are likely to have a pattern of endogenous sex hormones (higher E2, lower T, higher E2/T ratios) similar to those observed in young men with premature myocardial infarction.

Adult↗
PubMed1985

Apolipoprotein AI and AII metabolism in patients with primary high-density lipoprotein deficiency associated with familial hypertriglyceridemia.

Plasma high-density lipoproteins (HDL) and their major proteins--apolipoprotein (apo) AI and apo AII--are subnormal in most patients with familial hypertriglyceridemia. However, the pathophysiology of low-plasma apo AI and apo AII is unclear. The kinetic parameters (turnover) of HDL apo AI and apo AII were studied in six lean patients with primary HDL deficiency associated with familial hypertriglyceridemia and five normolipidemic controls. Autologous 125I labeled HDL were injected intravenously (IV; 25 microCi) and blood samples drawn ten minutes after the injection and periodically thereafter for 12 days. Urine samples were collected daily and their radioactivity measured. Kinetic parameters were calculated from the area under the decay curve using three exponentials. Mean plasma apo AI and apo AII were significantly lower (P less than 0.001) in patients than normals (70.4 +/- 2.7 v 106.9 +/- 7.0; 24.2 +/- 1.6 v 39.2 +/- 0.9 mg/dL, respectively). The mean fractional catabolic rates (FCR) obtained from plasma 125I-HDL, apo AI, apo AII radioactivity decay curves and by Berson and Yalow's method (urine/plasma radioactivity ratios) were significantly greater (P less than 0.05) in patients than in controls (0.387 v 0.299; 0.391 v 0.309; 0.361 v 0.275; 0.272 v 0.207/d; respectively). The mean synthetic rates (SR) of apo AI and apo AII were significantly lower in patients than in controls (11.12 v 14.17 mg/kg body weight/d, P less than 0.05; 3.53 v 4.68 mg/kg body weight/d, P less than 0.05, respectively). In vitro lipolysis of triglyceride (TG) rich lipoproteins by bovine lipoprotein lipase, and measurement of hepatic TG lipase and lipoprotein lipase in postheparin plasma were similar in patients and controls, indicating no abnormality in these factors that are linked to HDL and TG catabolism. However, a significant positive correlation between hepatic TG lipase and the FCR of apo AI and apo AII was found. The data suggest that in this series of patients with HDL deficiency the low plasma HDL-cholesterol, apo AI, and apo AII levels resulted from decreased synthesis and an increased fractional catabolic rate of apo AI and apo AII, the major proteins of HDL.

Adult↗
PubMed1983

Estradiol, testosterone, apolipoproteins, lipoprotein cholesterol, and lipolytic enzymes in men with premature myocardial infarction and angiographically assessed coronary occlusion.

A series of thirty-three Venezuelan men with premature myocardial infarction (mean age (M +/- SEM) 45 +/- 1.5 yrs) and with greater than 50% occlusion of at least 2 coronary arteries, and 19 weight matched control men (age 44 +/- 2 yrs) with normal coronary arteries on coronary angiography were studied. The percentages of significantly abnormal (greater than +/- 2 S.D. of controls) serum or plasma concentrations of various measurements (in decreasing order) were: estradiol (33%), total apolipoprotein (apo)B (24%), estradiol/testosterone ratio (21%), low density lipoprotein (LDL) apo B (19%), apo AI (17%), apo AI/total plasma apo B ratio (17%), total cholesterol (17%), and LDL-cholesterol (LDL-C) (11%). In addition, a multivariate discriminant function analysis showed that only estradiol, apo AI, LDL-C, estradiol/testosterone ratio and total cholesterol were statistically significant independent markers of myocardial infarction with occlusive coronary disease in these patients. Both serum estradiol and estradiol/testosterone ratio correlated positively with plasma apo B and LDL apo B, and inversely with apo AI; serum testosterone correlated inversely with plasma apo B (p less than 0.05). The data suggest that circulating sex hormones (estrogens, testosterone) are not only independent markers of coronary disease but may be pathogenetically linked to apo B and apo AI metabolism.

Adult↗