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Biomedical subjects

M de Courten

Publications and source records attributed to M de Courten.

At least 19 recordsLinked to original sources
PubMed2005

Increasing prevalence of Type 2 diabetes mellitus in all ethnic groups in Mauritius.

AIMS: To describe the prevalence of different stages of glucose intolerance in a population from Mauritius followed over 11 years. METHODS: Population-based surveys were undertaken in the multiethnic nation of Mauritius in 1987, 1992 and 1998, with 5083, 6616, and 6291 participants, respectively. Questionnaires, anthropometric measurements, and a 2-h 75-g oral glucose tolerance test were included. Subjects aged between 25 and 75 years with classifiable data were identified; 4991, 6463 and 5392 from 1987, 1992 and 1998, respectively. Glucose tolerance was classified according to WHO 1999 criteria. RESULTS: The prevalence of Type 2 diabetes increased significantly during the period studied, from 12.8% in 1987, to 15.2% in 1992, and 17.9% in 1998. The increasing prevalence was seen in both men and women, and in all age groups. The prevalence of known diabetes (KDM) increased progressively, and more markedly than the increase in newly diagnosed diabetes (NDM). A diagnosis of impaired glucose tolerance (IGT) was more prevalent amongst women whereas impaired fasting glucose (IFG) was more common amongst men. The prevalences of IGT and IFG did not change markedly during the period. The prevalence of diabetes and IGT was similar for participants of Indian, Creole and Chinese background in each survey, and the increasing prevalence of diabetes was seen in all ethnic groups. CONCLUSION: In this study, we report an increasing prevalence of diabetes over an 11-year period in Mauritius. This increase was seen in both sexes, and in all age and ethnic groups, and was mainly due to an increase in the numbers of those with known diabetes.

Adult↗
PubMed2004

High incidence of type 2 diabetes and increasing conversion rates from impaired fasting glucose and impaired glucose tolerance to diabetes in Mauritius.

OBJECTIVE: To describe the incidence of different stages of glucose intolerance in a population from Mauritius followed over 11 years. RESEARCH DESIGN, METHODS AND SUBJECTS: Population-based surveys were undertaken in the multi-ethnic nation of Mauritius in 1987, 1992 and 1998 with 5083, 6616 and 6291 participants, respectively. Questionnaires, anthropometric measurements, and a 2-h 75-g oral glucose tolerance test were included. Three cohorts aged between 25 and 79 years with classifiable glucose tolerance data were identified; 3680 between 1987 and 1992, 4178 between 1992 and 1998, and 2631 between 1987 and 1998. Glucose tolerance was classified according to WHO 1999 criteria. RESULTS: The incidence rate of type 2 diabetes was higher between 1992 and 1998 than between 1987 and 1992. In men, the incidence was similar between cohorts (24.5 and 25.4 per 1000 person-years) whereas the incidence increased in women (23.3 and 16.4 per 1000 person-years). The incidence of diabetes peaked in the 45-54 year age group and then plateaued or fell. The incidences of impaired glucose tolerance (IGT) and impaired fasting glucose (IFG) decreased in both men and women. Of normoglycaemic subjects at baseline, more women than men developed IGT and more men than women developed IFG. Of those labelled as IFG in 1987, 38% developed diabetes after 11 years. The corresponding figure for IGT was 46%. CONCLUSIONS: In this study, we report changes in incidence rates of glucose intolerance over a 11-year period. In particular, differences between men and women were observed. The increased incidence of IGT in women compared with men, and increased incidence of IFG in men compared with women was consistent with, and explains the sex biases seen in the prevalences of these states.

Adult↗
PubMed2001

Leptin and other components of the Metabolic Syndrome in Mauritius--a factor analysis.

OBJECTIVE: To use factor analysis to examine the putative role of leptin in the Metabolic Syndrome, and to define better the associations among observed variables and the identified factors. DESIGN: Factor analysis of cross-sectional data from a 1987 survey. SUBJECTS: Non-diabetic residents of Mauritius who participated in population-based surveys in 1987 and 1992 (1414 men and 1654 women). MEASUREMENTS: Fasting and 2 h plasma glucose and insulin following a 75 g oral glucose load; seated blood pressure; body mass index (BMI); waist-to-hip ratio (WHR); and fasting serum triglycerides, HDL-cholesterol, leptin and uric acid concentrations. RESULTS: Principal components factor analysis revealed three factors for men and women that explained between 54 and 55% of the observed variance of the 12 measured variables. General features of these factors were as follows: factor 1, WHR, BMI, leptin, fasting and 2 h insulin, triglycerides, and HDL-cholesterol; factor 2, systolic and diastolic blood pressure, uric acid (men only), and fasting glucose (women only); and factor 3, fasting and 2 h glucose and insulin. Only three variables loaded on more than one factor with a loading > or = 0.4 (fasting and 2 h insulin, fasting glucose in women only). Leptin loaded on one factor only in both men and women. CONCLUSIONS: Since multiple factors underlie the Metabolic Syndrome, and since no observed variable loads on all three factors, more than one mechanism might account for the observed clustering of risk characteristics. Leptin does not unite features of this syndrome due to its loading on one factor only. Uric acid is related to a different factor in men and women. The absence of gender differences in factor loadings argues for similar mechanisms for the Metabolic Syndrome in men and women in Mauritius. International Journal of Obesity (2001) 25, 126-131

Adult↗
PubMed2000

Impaired fasting glucose: how low should it go?

OBJECTIVE: Impaired fasting glucose (IFG) has been recently introduced as a stage of abnormal carbohydrate metabolism, but the evidence on which its glucose limits (fasting plasma glucose [FPG] 6.1-6.9 mmol/l) are based is not strong. The aim of this study was to determine if 6.1 mmol/l represents a clear cutoff in terms of the risk of future diabetes and in terms of elevated cardiovascular risk factor levels, and to examine the use of other lower limits of IFG. RESEARCH DESIGN AND METHODS: A population-based survey of the island of Mauritius was undertaken in 1987, with a follow-up survey 5 years later. On both occasions, an oral glucose tolerance test was performed and cardiovascular risk factors were measured. RESULTS: Data were available from 4,721 nondiabetic people at baseline, and from 3,542 at follow-up. At baseline, blood pressure, lipids, and obesity increased in a linear fashion with increasing FPG, with no evidence of a threshold effect. The risk of developing hypertension at follow-up was greater for those people with baseline FPG > or =6.1 mmol/l (P<0.001). The risk of developing diabetes at follow-up increased with increasing baseline FPG, but there was little evidence of a threshold near 6.1 mmol/l. CONCLUSIONS: Cardiovascular risk and risk of future diabetes increase continually with increasing FPG, and there is no threshold value on which to base a definition of IFG. If a lower limit of approximately 5.8 mmol/l is used, the category defines a group more similar to the group with impaired glucose tolerance, with regard to total prevalence and the risk of subsequent diabetes.

Adult↗
PubMed2000

Features of the metabolic syndrome predict higher risk of diabetes and impaired glucose tolerance: a prospective study in Mauritius.

OBJECTIVE: To assess the independent and joint effects of the components of the metabolic syndrome, including leptin, which is a recently proposed addition to this syndrome, in predicting the cumulative incidence of impaired glucose tolerance (IGT) and diabetes among individuals with normal glucose tolerance. RESEARCH DESIGN AND METHODS: This prospective study involved 2,605 residents of Mauritius with normal glucose tolerance who were followed for 5 years for IGT or diabetes onset in relation to total and regional adiposity (BMI, waist-to-hip ratio [WHR]), fasting and 2-h 75-g oral glucose load glucose and insulin, total and HDL cholesterol, blood pressure, serum uric acid, triglyceride, and leptin levels. RESULTS: A multivariate logistic regression model adjusted for age, sex, ethnicity, and diabetes family history showed a significantly higher linear increase in risk of IGT and diabetes in association with the following variables only: fasting glucose (odds ratio 1.89 [95% CI 1.51-2.34]), 2-h glucose (1.68 [1.50-1.88]), WHR (1.30 [1.10-1.52]), BMI (1.04 [1.00-1.08]), and serum uric acid (1.37 [1.20-1.57]). However, a nonlinear increase was seen with serum triglyceride and plasma leptin concentrations. No risk factors resulted in joint effects that were greater than expected from combining individual effects. CONCLUSIONS: Metabolic syndrome features independently predict a higher risk of diabetes or IGT in normoglycemic subjects but in combination confer no higher-than-expected risk of these outcomes. At higher concentrations of triglycerides and leptin, risk plateaus and even declines slightly.

Adult↗
PubMed2000

Type 2 diabetes worldwide according to the new classification and criteria.

Two major reports have recently revised the classification of and diagnostic criteria for diabetes. Classification was previously based on the need for insulin (insulin-dependent or non-insulin-dependent), but this has become increasingly confusing. Now, the type of diabetes is determined by the etiological process rather than the treatment modality. Type 1 diabetes is thus characterized by islet cell destruction and type 2 diabetes by a combination of defects in insulin secretion and action. An individual with either type of diabetes may be on any treatment modality. This classification should prove to be more logical and, for example, allow latent autoimmune diabetes in adults, which typically does not require insulin at presentation, to be classified as type 1 diabetes. The fasting plasma glucose diagnostic threshold for diabetes has been lowered to 7.0 mmol/l (126 mg/dl), and impaired fasting glucose (fasting plasma glucose 6.1-6.9 mmol/l [110-125 mg/dl]) has been introduced as a new category of intermediate glucose metabolism. These changes recognize that the old fasting threshold did not match the 2-h (postload) threshold well and that both micro- and macrovascular disease develop at lower fasting glucose levels than previously recognized. Although the prevalences of diabetes according to the new fasting and 2-h criteria are now similar in most populations, the actual individuals identified as having diabetes are often different. Over 30% of all those with diabetes have a nondiabetic fasting glucose but still have increased cardiovascular mortality. Thus, it is important to retain the oral glucose tolerance test for the diagnosis of diabetes.

Blood Glucose↗
PubMed1999

Etiology of the metabolic syndrome: potential role of insulin resistance, leptin resistance, and other players.

Obesity and Type 2 diabetes are now major public health issues in developed nations and have reached epidemic proportions in many developing nations, as well as disadvantaged groups in developed countries, e.g., Mexican-Americans, African-Americans, and Australian Aborigines. These groups all show hyperinsulinemia and insulin resistance, which have been demonstrated to be future predictors of Type 2 diabetes and have also been suggested as key factors in the etiology of the Metabolic Syndrome. It is now increasingly recognized that Type 2 diabetes is part of a cluster of cardiovascular disease (CVD) risk factors comprising the Metabolic Syndrome. This group is at very high risk of atherosclerosis because each of the risk factors in the Metabolic Syndrome cluster in its own right is an important CVD risk factor. They also contribute cumulatively to atherosclerosis. A key strategy in reducing macrovascular disease lies in the better understanding of the Metabolic Syndrome--glucose intolerance, hypertension, hyperlipidemia, and central obesity. Although it has been suggested that hyperinsulinemia/insulin resistance is the central etiological factor for the Metabolic Syndrome, epidemiological data do not support the idea that this can account for all of the cluster abnormalities. We have animal and human data suggesting that hyperleptinemia rather than, or synergistically with, hyperinsulinemia may play a central role in the genesis of the CVD risk factor cluster that constitutes the syndrome. Studies in Psammomys obesus (the Israeli sand rat) suggest hyperinsulinemia/insulin resistance is an early metabolic lesion in the development of obesity and Type 2 diabetes. This animal also develops other features of the Metabolic Syndrome, making it an excellent model to investigate etiology. Psammomys, when placed on an ad libitum laboratory diet, develops hyperinsulinemia, insulin resistance, impaired glucose tolerance, diabetes, and dyslipidemia. It also develops hyperleptinemia and leptin insensitivity, and hyperleptinemia is correlated with insulin resistance independent of changes in body weight. It is likely that a similar sequence occurs in the transition from the prediabetic state to Type 2 diabetes in humans. More recently, other potential players in the etiology of the Metabolic Syndrome have been suggested including endothelial dysfunction and acetylation-stimulating protein (ASP). It has been suggested that endothelial dysfunction may be an antecedent for both Type 2 diabetes and the Metabolic Syndrome. In addition, ASP is a serious new candidate for an important role in insulin resistance. The ASP pathway plays a critical role in fatty acid metabolism and storage, and it has been suggested that ineffective storage of fatty acids by adipocytes due to a defect in the ASP pathway may lead to insulin resistance and Type 2 diabetes.

Acetylation↗
PubMed1999

Isolated post-challenge hyperglycaemia confirmed as a risk factor for mortality.

AIMS/HYPOTHESIS: The aim of this study was to examine the possible link between isolated post-challenge hyperglycaemia (2-h post-challenge plasma glucose >/= 11.1 mmol/l, and fasting plasma glucose < 7.0 mmol/l) and mortality. METHODS: The data from three population based longitudinal studies (in Mauritius, Fiji and Nauru) were pooled and mortality rates were determined in 9179 people who were followed for between 5 and 12 years. RESULTS: There were 595 people with previously diagnosed diabetes, and 799 with newly diagnosed diabetes, of whom 243 (31) had isolated post-challenge hyperglycaemia. In comparison with people without diabetes, people with isolated post-challenge hyperglycaemia had an increased risk of all-cause mortality [Cox proportional hazards ratio (95 % CI): 2.7 (1.8-3.9) - men; 2.0 (1.3-3.3) - women], and of cardiovascular mortality [2.3 (1.2-4.2) - men; 2.6 (1.3-5.1) - women]. In addition, men with isolated post-challenge hyperglycaemia had a high risk of cancer death [8.0 (3.6-17.9)]. CONCLUSION/INTERPRETATION: These data show that isolated post-challenge hyperglycaemia, which can only be identified by the 2-h glucose, is common, and at least doubles the mortality risk. This should be considered in the design of screening programmes that use only fasting glucose.

Adult↗
PubMed1999

Impaired fasting glucose or impaired glucose tolerance. What best predicts future diabetes in Mauritius?

OBJECTIVE: To determine if impaired fasting glucose (IFG; fasting plasma glucose level 6.1-6.9 mmol/l) can predict future type 2 diabetes as accurately as does impaired glucose tolerance (IGT; 2-h plasma glucose level 7.8-11.0 mmol/l). RESEARCH DESIGN AND METHODS: A longitudinal population-based study was performed with surveys in 1987 and 1992 on the island of Mauritius, assessing diabetes status by the oral glucose tolerance test. A total of 3,717 subjects took part in both surveys. Of these subjects, 3,229 were not diabetic in 1987 and formed the basis of this study. RESULTS: At baseline, there were 607 subjects with IGT and 266 subjects with IFG. There were 297 subjects who developed diabetes by 1992. For predicting progression to type 2 diabetes, the sensitivity, specificity, and positive predictive values were 26, 94, and 29% for IFG and 50, 84, and 24% for IGT, respectively. Only 26% of subjects that progressed to type 2 diabetes were predicted by their IFG values, but a further 35% could be identified by also considering IGT. The sensitivities were 24% for IFG and 37% for IGT in men and 26% for IFG and 66% for IGT in women, respectively. CONCLUSIONS: These data demonstrate the higher sensitivity of IGT over IFG for predicting progression to type 2 diabetes. Screening by the criteria for IFG alone would identify fewer people who subsequently progress to type 2 diabetes than would the oral glucose tolerance test.

Adult↗
PubMed1999

Impact of new diagnostic criteria for diabetes on different populations.

OBJECTIVE: For epidemiological purposes, it has now been recommended that a fasting plasma glucose value of 7.0 mmol/l can be used to diagnose diabetes, instead of a 2-h value of 11.1 mmol/l. This study assesses the impact of making this change on the prevalence of diabetes and on the phenotype of individuals identified. RESEARCH DESIGN AND METHODS: Data were collated from nine population based southern hemisphere studies in which a 75-g oral glucose tolerance test was performed. Comparisons were made between the prevalence derived from fasting values only and the prevalence derived from 2-h values only. Cardiovascular risk was assessed in all individuals. RESULTS: There were 20,624 subjects in the nine surveys of whom 1,036 had previously diagnosed diabetes and 1,714 had newly diagnosed diabetes, according to either fasting or 2-h glucose. The differences in prevalence within each population resulting from changing the diagnostic criteria ranged from +30 to -19% (relative difference) and +4.1 percentage points to -2.8 percentage points (absolute difference). BMI was the most important determinant of disagreement in classification. A total of 31% of those individuals who were diabetic on the fasting value were not diabetic on the 2-h value, and 32% of those with diabetes on the 2-h value were not diabetic on the fasting value. Apart from obesity, there were no differences in cardiovascular risk between those identified by the fasting and the 2-h values. CONCLUSIONS: Changing the diagnostic criteria is likely to have variable and sometimes quite large effects on the prevalence of diabetes in different populations. Furthermore, the fasting criterion identifies different people as being diabetic than those identified by the 2-h criterion.

Adult↗
PubMed1998

Diabetic neuropathy in Mauritius: prevalence and risk factors.

The study of diabetic neuropathy has been primarily in Europids, despite the high prevalence of diabetes in other populations. We set out to ascertain the prevalence of diabetic neuropathy and its risk factors in the island nation of Mauritius. Population surveys were carried out in 1987 and 1992 in Mauritius to establish the prevalence of Type 2 diabetes. In the second survey, vibration perception threshold (VPT) was also measured at the great toe in 847 subjects with diabetes, 204 subjects with impaired glucose tolerance and 127 subjects with normal glucose tolerance. Neuropathy was defined as levels of VPT exceeding the mean plus 2 standard deviations defined separately for three age groups of Mauritian non-diabetic subjects. Risk factors for neuropathy were identified cross sectionally from the 1992 data, and longitudinally from the 1987 data. Neuropathy was detected in 8.3% of the 847 diabetic subjects (12.7%) of those with known diabetes, and 3.6% of those with newly diagnosed diabetes). Logistic regression identified diabetes duration (odds ratio [95% CI]; 1.08 [1.04-1.13] per year, P=0.0002), treatment with insulin or oral hypoglycaemic agents (2.63 [1.36-5.09], P=0.004) and greater height (1.36 [1.19-1.57] per 5 cm, P < 0.001) as risk factors for neuropathy, in the cross sectional analysis. In the longitudinal analysis, diabetes duration (1.11 [1.05-1.18] per year, P=0.001), fasting glucose (1.12 [1.03-1.22] per mmol/l, P=0.01) and height (1.23 [1.03-1.45] per 5 cm, P=0.02) were associated with neuropathy. A lower 2-h plasma insulin was also associated with neuropathy in the longitudinal analysis. The prevalence of diabetic neuropathy in Mauritius is the lowest reported for any population, but the risk factors associated with it are similar to those previously found.

Adult↗
PubMed1997

Hyperleptinaemia: the missing link in the, metabolic syndrome?

Leptin's association with fasting insulin raises the possibility that hyperleptinaemia is an additional component of the Metabolic Syndrome, or perhaps underlies the syndrome. This population-based study of Western Samoans examined the relationship of serum leptin with insulin sensitivity assessed by Homeostatic Model Assessment (HOMA) and components of the Metabolic Syndrome. Two hundred and forty subjects (114 men, 126 women), aged 28-74 years, were drawn from a study conducted in 1991. An oral glucose tolerance test indicated that 59 subjects had diabetes. Diabetic men had higher leptin levels than non-diabetic (6.0 vs 3.2 ng ml-1) but this difference was no longer significant after adjustment for BMI. Leptin levels in diabetic women (24.7 ng ml-1) non-diabetic women (22.6 ng ml-1) were not different. Leptin was strongly, positively correlated with BMI, fasting insulin and mean blood pressure after adjusting for age and sex (r > 0.43, p < 0.001), irrespective of glucose tolerance status. Linear regression models indicated that leptin was associated with insulin sensitivity independent of age, BMI, waist/hip ratio, triglycerides, HDL-cholesterol, and hypertension. Similar models were computed with mean blood pressure or triglycerides as the dependent variable, and including insulin sensitivity with the independent variables. Leptin was independently associated with mean blood pressure in men, but was not independently associated with triglycerides. Mean levels of 2-h insulin, triglycerides, LDL-cholesterol, and systolic blood pressure varied across tertiles of leptin in men after adjusting for age, BMI, and insulin sensitivity, and mean levels in the top tertile tended to be higher than in the lowest tertile. These results indicate an independent relationship between leptin and insulin sensitivity, but the equivocal results concerning associations of leptin with components of the Metabolic Syndrome make it unlikely that leptin affects these directly.

Adult↗
PubMed1997

Fasting hyperinsulinemia is a predictor of increased body weight gain and obesity in Pima Indian children.

Hyperinsulinemia is commonly associated with obesity, but it has not been determined which defect comes first. Some have proposed that hyperinsulinemia may precede obesity in populations prone to NIDDM, such as Pima Indians or Pacific Islanders. In contrast, longitudinal studies in adults show that insulin sensitivity and low fasting insulin concentrations are associated with increased weight gain, whereas insulin resistance seems to protect against weight gain. The present study examined whether fasting plasma hyperinsulinemia is a risk factor for weight gain in prepubertal children in the Pima Indian population-a population that is prone to obesity. Fasting plasma insulin concentration was measured in 328 5- to 9-year-old Pima Indian children (147 boys and 181 girls) with normal glucose tolerance. Follow-up weight was obtained an average of 9.3 +/- 1.9 years (means +/- SD) later at age 15-19 years. Fasting plasma insulin concentration correlated with the rate of weight gain per year in both boys (r = 0.42; P < 0.0001) and girls (r = 0.20; P < 0.01) and was associated with the rate of weight gain, independent of known determinants of weight change, i.e., initial relative weight, change in height, age, and sex. Similar relationships were found between fasting plasma insulin concentration and the change in relative weight and in triceps skinfold thickness-two indicators of obesity. In conclusion, fasting hyperinsulinemia may be a risk factor for the development of obesity in young children.

Arizona↗
PubMed1996

Serum leptin concentration, obesity, and insulin resistance in Western Samoans: cross sectional study.

OBJECTIVE: To measure serum leptin concentrations in the Polynesian population of Western Samoa and to examine epidemiological associations of leptin with anthropometric, demographic, behavioural, and metabolic factors in this population with a high prevalence of obesity and non-insulin dependent diabetes mellitus. DESIGN: Cross sectional study, leptin concentration being measured in a subgroup of a population based sample. SUBJECTS: 240 Polynesian men and women aged 28-74 years were selected to cover the full range of age, body mass index, and glucose tolerance. MAIN OUTCOME MEASUREMENTS: Serum leptin, insulin, and glucose concentrations; anthropometric measures; physical activity; and area of residence. RESULTS: Leptin concentrations were correlated with body mass index (r = 0.80 in men, 0.79 in women) and waist circumference (r = 0.82 in men, 0.78 in women) but less so with waist to hip ratio. At any body mass index, leptin concentration was higher in women than men (geometric mean adjusted for body mass index 15.3 v 3.6 pg/l, P < 0.001). Leptin concentration also correlated with fasting insulin concentration (r = 0.63 in men, 0.64 in women) and insulin concentration 2 hours after a glucose load (r = 0.58 in men, 0.52 in women). These associations remained significant after controlling for body mass index; effects of physical activity and of rural or urban living on leptin concentration were eliminated after adjusting for obesity, except values remained high in urban men. 78% of variance in leptin was explained by a model including fasting insulin concentration, sex, body mass index, and a body mass index by sex interaction term. Similar results were obtained if waist circumference replaced body mass index. CONCLUSIONS: The strong relation of leptin with obesity is consistent with leptin production being proportional of mass to adipose tissue. The relation with insulin independent of body mass index suggests a possible role for leptin in insulin resistance or hyperinsulinaemia.

Adult↗
PubMed1995

Lisinopril is neutral to insulin sensitivity and serum lipoproteins in essential hypertensive patients.

To investigate the effects of antihypertensive treatment with the angiotensin-converting enzyme (ACE) inhibitor lisinopril on insulin sensitivity and related metabolic variables, the insulin sensitivity index (SI), determined with the Minimal Model Method of Bergman, fasting plasma insulin and glucose concentrations, serum total triglyceride and lipoprotein cholesterol fractions, and blood pressure were assessed in 24 lean, non-diabetic patients with essential hypertension. Following a double-blind, randomised crossover design, these parameters were measured after a 4-week run-in period, after 8 weeks of lisinopril or placebo, and after an additional 8 weeks on placebo or lisinopril, respectively. Furthermore, the level of physical fitness was estimated using the Conconi bicycle ergometer test. SI was low in this study population (5.6 vs 13.3 x 10(-4).min-1.mU-1.l-1 in normal lean control subjects). It did not differ between the placebo run-in phase, the lisinopril phase, and the placebo crossover phase (5.8, 5.5, and 5.4 x 10(-4).min-1.mU-1.l-1, respectively). Moreover, during the administration of lisinopril, no significant changes occurred in fasting plasma insulin and glucose, areas under the glucose and insulin curves, glucose disappearance rate, serum total triglycerides, and cholesterol or lipoprotein cholesterol fractions. Heart rate at rest, body weight, and anaerobic threshold remained stable throughout the study. Compliance assessed by pill-counting exceeded 90% at all visits. These findings demonstrate that the ACE inhibitor lisinopril is neutral with regard to insulin sensitivity, plasma insulin and glucose, and lipoprotein metabolism in patients with essential hypertension.

Adult↗
PubMed1995

Insulin resistance and hyperinsulinemia in hypertension.

GENETIC PREDISPOSITION: Insulin resistance and reactive hyperinsulinemia occur not only with obesity, impaired glucose tolerance or non-insulin-dependent (type 2) diabetes mellitus, but also in many non-obese, non-diabetic patients with essential hypertension and their currently normotensive, lean, young offspring, as well as in some other conditions known to promote hypertension. Insulin resistance impairs glucose tolerance, while insulin resistance and/or hyperinsulinemia promote dyslipidemia, body fat deposition and probably atherogenesis. Therefore, the common coexistence of a genetic predisposition for hypertension with insulin resistance helps to explain the frequent, although temporally often dissociated, occurrence of hypertension together with dyslipidemia, obesity and type 2 diabetes in a given patient. INSULIN RESISTANCE AND HYPERINSULINEMIA AS SLOW PRESSOR MECHANISMS: In the pathogenesis of hypertension, inappropriate vasoconstriction (due to an imbalance of vasoactive substances and/or raised cytosolic calcium) and/or structural vasculopathy is particularly important. Among the mosaic of assumed pressor mechanisms, distinct Na+ retention is almost invariably involved in diabetes mellitus, while sympathetic activation tends to occur in essential hypertension, particularly in association with obesity. Insulin resistance may develop as a consequence of an intracellular excess of Ca2+ or a decrease in Mg2+, an impaired insulin-mediated rise in skeletal muscle blood flow, increased sympathetic activity or excess body weight. Acute hyperinsulinemia causes arterial vasodilation on one hand and increases sympathetic activity and renal Na+ reabsorption on the other. Chronically, hyperinsulinemia may promote cardiovascular muscle cell proliferation and atherogenesis, while insulin resistance may be associated with certain transmembraneous cation transporters, leading to an increase in cytosolic Ca2+. Hyperinsulinemia and/or insulin resistance may also be associated with an increased blood pressure sensitivity to high salt intake. In the mosaic of many different blood pressure-raising mechanisms, insulin resistance and/or hyperinsulinemia is likely to represent an amplifying slow or very slow pressor factor.

Coronary Disease↗