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Biomedical subjects

K G Alberti

Publications and source records attributed to K G Alberti.

At least 73 records · Page 4Linked to original sources
PubMed1998

Do leptin levels predict weight gain?--A 5-year follow-up study in Mauritius. Mauritius Non-communicable Disease Study Group.

OBJECTIVE: To investigate whether relative baseline leptin levels predict long-term changes in adiposity and/or its distribution. RESEARCH METHODS AND PROCEDURES: In a longitudinal study of 2888 nondiabetic Mauritians aged 25 years to 74 years who participated in population-based surveys in 1987 and 1992, changes in body mass index (BMI), waist/hip ratio (WHR), and waist circumference were compared between "hyperleptinemic," "normoleptinemic," and "hypoleptinemic" groups. "Relative leptin levels" were calculated as standardized residuals from the regression of log10 leptin on baseline BMI to provide a leptin measure independent of BMI. Analyses were performed within each sex. A linear regression model was used to assess the effect of standardized residuals on changes in BMI, WHR, and waist circumference, independent of baseline BMI, age, fasting insulin, and ethnicity. RESULTS: After adjusting for age and baseline BMI by analysis of covariance, there was no difference in changes in BMI, WHR, or waist circumference between men with low, normal, or high relative leptin levels. Among women, there was a significant difference in deltaWHR across leptin groups, such that the largest increase occurred in the "normal" leptin group. For both men and women, the linear regression models explained approximately 10% of variation in dependent variables, and the only significant independent variables were age, BMI, and being of Chinese origin, compared with Indian origin. DISCUSSION: These findings do not support a role for leptin concentration in predicting weight gain or changes in fat distribution in adults over a 5-year period.

Blood Glucose↗
PubMed1998

Long-term effects of a sustained-release preparation of acipimox on dyslipidemia and glucose metabolism in non-insulin-dependent diabetes mellitus.

Elevated circulating plasma nonesterified fatty acids (NEFA) may contribute to the insulin resistance and hyperglycemia of non-insulin-dependent diabetes mellitus (NIDDM), and decreasing plasma NEFA could provide a therapeutic benefit. A sustained-release preparation of acipimox, a lipolysis inhibitor, was used in an attempt to decrease circulating plasma NEFA levels long-term, and the effects on glycemic control, insulin resistance, and serum lipids were measured. Sixty NIDDM patients (43 males and 17 females) took part in a randomized controlled trial of acipimox or placebo for 12 weeks. Fasting plasma NEFA levels did not change in acipimox-treated patients (baseline v 12 weeks, 0.84 +/- 0.35 v 0.88 +/- 0.55 mmol x L(-1), mean +/- SD). Fasting blood glucose was unchanged (mean difference v placebo, -0.5 mmol x L(-1); 95% confidence interval [CI], -1.4 to 0.3 mmol x L[-1]), but serum fructosamine decreased (mean difference v placebo, -26 micromol x L(-1); 95% CI, -51 to 0 mmol x L[-1]), as did the standardized hemoglobin A1 ([HbA1] mean difference v placebo, -1.4%; 95% CI, -3.0% to -0.1%). Insulin resistance measured as steady-state plasma glucose during an insulin-dextrose infusion test was unchanged (mean difference v placebo, -1.4 mmol x L(-1); 95% CI, -3.2 to 0.5 mmol x L[-1]). Serum total cholesterol (mean difference v placebo, -0.4 mmol x L(-1); 95% CI, -0.6 to -0.1 mmol x L[-1]), serum apolipoprotein B ([apo B] mean difference v placebo, -0.19 g x L(-1); 95% CI, -0.3 to -0.1 g x L[-1]), and serum triglycerides (mean difference v placebo for pretreatment v posttreatment ratio, 0.59; 95% CI, 0.40 to 0.88) were all lower with acipimox. Serum high-density lipoprotein (HDL) cholesterol (mean difference v placebo, 0.10 mmol x L(-1); 95% CI, -0.05 to 0.3 mmol x L[-1]), serum apo A1 (mean difference v placebo, 0.03 g x L(-1); 95% CI, -0.04 to 0.1 g x L[-1]), and serum lipoprotein(a) ([Lp(a)] acipimox v placebo, 154 (0 to 1,574) v 71 (0 to 1,009), median and range) were unchanged. Despite the lack of change in fasting plasma NEFA levels, acipimox caused a modest beneficial improvement in overall glycemic control and plasma lipids in NIDDM patients and could be a useful agent in the treatment of dyslipidemic NIDDM patients.

Apolipoprotein A-I↗
PubMed1998

Impaired glucose tolerance: what are the clinical implications?

Impaired glucose tolerance (IGT) was standardized in 1979 by the National Diabetes Data Group and the World Health Organization as a risk factor for type 2 diabetes, replacing groups such as 'borderline' and 'chemical' diabetes. IGT was defined by a blood/plasma glucose value 2 h after a 75 g glucose load that was clearly abnormal but did not convey a risk of microangiopathy in those with non-diabetic fasting blood/plasma glucose levels. IGT is not uncommon, having a prevalence of 2-25% in adults. Determinants include age, obesity (total and central), family history of type 2 diabetes, physical inactivity and triglyceride levels. The main clinical significance of IGT is: (1) as a risk factor for type 2 diabetes, with 20-50% of individuals developing type 2 diabetes over 10 years; (2) as a risk factor for cardiovascular disease (CVD); and (3) as a component of the metabolic syndrome. IGT can be treated and this may prevent or delay progression to type 2 diabetes, though the effect of treatment on the risk of CVD is unknown.

Cardiovascular Diseases↗
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↗
PubMed1998

Is there a relationship between leptin and insulin sensitivity independent of obesity? A population-based study in the Indian Ocean nation of Mauritius. Mauritius NCD Study Group.

OBJECTIVE: It has been shown previously in smaller studies that fasting serum leptin and insulin concentrations are highly correlated, and insulin sensitive men have lower leptin levels than insulin resistant men matched for fat mass. We have examined the association between insulin resistance (assessed by fasting insulin) and leptin after controlling for overall and central adiposity in a population-based cohort. DESIGN: Leptin levels were compared across insulin resistance quartiles within three categories of obesity (tertiles of body mass index (BMI)). Partial correlation coefficents and multiple linear regression models were used to assess the relationship between leptin and fasting insulin after adjusting for BMI and waist to hip ratio (WHR) or waist circumference. SUBJECTS: Subjects were normoglycemic participants of a 1987 non-communicable diseases survey conducted in the multiethnic population of Mauritius. 1227 men and 1310 women of Asian Indian, Creole and Chinese ethnicity had normal glucose tolerance and fasting serum leptin measurements. RESULTS: Mean serum leptin concentration increased across quartiles of fasting insulin in each BMI group and gender, after controlling for BMI, WHR and age. Furthermore, fasting insulin was a significant determinant of serum leptin concentration, independent of BMI and WHR, in both men and women. Similar results were found if waist circumference replaced BMI and WHR in the model. CONCLUSION: These results suggest that insulin resistance/concentration may contribute to the relatively wide variation in leptin levels seen at similar levels of body mass or alternatively, leptin may play a role in the etiology of insulin resistance. Further studies will be important to determine whether the hyperleptinemia/insulin resistance relationship has a role in the natural history of obesity, Type 2 diabetes mellitus and the other metabolic abnormalities associated with insulin resistance.

Adult↗
PubMed1998

Acute effects on insulin sensitivity and diurnal metabolic profiles of a high-sucrose compared with a high-starch diet.

Decreased insulin sensitivity is associated with diabetes mellitus, ischemic heart disease, and hypertension, both independently and in association as what is called the metabolic syndrome. Although the negative effects of obesity, sedentary lifestyles, and high-fat diets on insulin sensitivity are well established, the influence of type and quantity of dietary carbohydrate is more controversial. This study aimed to assess the acute (24 h) effects of a high-sucrose compared with a high-starch diet on insulin sensitivity and to identify changes in blood metabolites that might lead to altered insulin sensitivity. Eight healthy adults consumed high-sucrose or high-starch diets (50% of dietary energy) in a randomized, crossover trial. Insulin sensitivity was assessed by a short insulin tolerance test the following morning. No differences were detected in insulin sensitivity, either for glucose metabolism [Kitt(glucose) (the rate constant for the decline in blood glucose concentrations) for sucrose diet = 3.86%/min, for starch diet = 3.72%/min; pooled SEM = 0.23] or for lipid metabolism [Kitt(NEFA) (the rate constant for the decline in blood fatty acid concentrations) for sucrose diet = 12.9%/min, for starch diet = 11.4%/min; pooled SEM = 1.18]. Profiles for blood glucose and serum insulin concentrations revealed higher peaks and lower troughs with the high-sucrose diet whereas area under the curve for glucose was higher with the high-starch diet (6780 +/- 245 mmol x L/min) than with the high-sucrose diet (6290 +/- 283 mmol x L/min) (P < 0.001). Plasma fatty acid concentrations showed a late postprandial rise with the sucrose-rich diet relative to the starch-rich diet, which was mirrored with a fractionally later peak in triacylglycerol concentrations.

Adult↗
PubMed1998

Insulin resistance and hypertension in non-obese Africans in Tanzania.

Insulin sensitivity was assessed using a glucose-insulin infusion test in 15 newly diagnosed non-obese hypertensive black Tanzanians with normal glucose tolerance and in 15 normotensive control subjects matched for age, sex, and body mass index. The steady-state blood glucose and metabolic clearance rate of glucose (MCR) were used as measures of insulin sensitivity. The mean MCR (glucose) was significantly reduced (7.12+/-0.57 versus 9.50+/-0.69 micromol/kg per minute; P<.05) and mean steady-state blood glucose was significantly elevated (5.0+/-0.3 versus 3.7+/-0.3 mmol/L; P<.01) in subjects with hypertension compared with the normotensive group. For all subjects there was a significant inverse correlation between MCR (glucose) and systolic (P=.003) and diastolic (P=.005) blood pressure; and a positive correlation was found between fasting serum insulin levels and systolic (P=.005) and diastolic (P=.004) blood pressure. These observations were independent of body mass index and serum lipid levels. These data indicate a strong association between insulin mediated glucose uptake and blood pressure in this population of normal weight untreated urban Africans.

Adult↗
PubMed1998

Early life and later determinants of adult disease: a 50 year follow-up study of the Newcastle Thousand Families cohort.

The relative contribution of socioeconomic, behavioural and biological factors operating in fetal and infant life, childhood and adulthood to risk for cardiovascular disease, respiratory diseases and non-insulin-dependent diabetes in middle age has become an important research issue. All 1142 babies born in Newcastle upon Tyne in May and June 1947 were recruited into a prospective cohort study of child health (the 'Thousand Families' study) and followed in great detail to the age of 15 y, with a brief further follow up at age 22 y. Children from poorer families were at greatest risk of severe respiratory tract infection in infancy. Children from professional and managerial families were on average taller and heavier throughout childhood than those from semi- and unskilled manual social classes. Repeated infections in early childhood greatly increased the risk of developing chronic respiratory disease by age 15 y. This paper outlines a new investigation designed to trace surviving members of this cohort and to chart the relationships between their socioeconomic circumstances, lifestyles, experiences and health from birth through to the present day. Existing data on socioeconomic circumstances and infections in infancy and childhood, infant nutrition, birthweight and physical development to age 22 y will be linked to information gained from a new study. This comprises a postal questionnaire survey of study members' adult health, socioeconomic circumstances and lifestyle, and a hospital based clinical examination including heart and lung function, glucose tolerance, blood lipids and anthropometric measurements at age 49-51 y. Out of a target sample of 979 people for whom sufficient data are available on the first year of life, 866 (88%) have been traced and 649 are still resident in the North of England. Those study members who have been traced are highly representative of the original cohort. The Thousand Families cohort provides a unique opportunity for detailed epidemiological study because of the wealth of data available on infant and childhood socioeconomic and family circumstances, all of which was collected prospectively. In addition, there has been comparatively little loss to follow-up since 1948.

Chi-Square Distribution↗
PubMed1997

Serum concentrations of vitamins A and E in impaired glucose tolerance.

Serum concentrations of vitamins A and E were measured in 32 subjects with impaired glucose tolerance (IGT) and 148 subjects with normal glucose tolerance using reversed-phase high-performance liquid chromatography. Fasting glucose, insulin and lipid concentrations were also measured. Serum vitamin A concentrations were higher in subjects with IGT 2.5 (1.1-3.4) vs. 2.1 (1.4-3.2) mumol/l [median (2.5-97.5 percentiles)] (P = 0.002), the difference remaining significant after adjustment for triglycerides (P = 0.028). There was a univariate association between vitamin A levels and insulin resistance (r = 0.164; P = 0.02) and in multivariate logistic regression analysis the relative risk of subjects with high vitamin A concentrations having IGT was 3.8 (P = 0.002). There were no differences in serum vitamin E concentrations between the groups. These data suggest that higher vitamin A concentrations found in non-insulin-dependent diabetes pre-date the onset of diabetes. Further studies are required to confirm this finding and to investigate the possibility of a role for vitamin A in the aetiology of diabetes and IGT.

Blood Glucose↗
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

Maternally inherited diabetes and deafness: prevalence in a hospital diabetic population.

Maternally inherited diabetes and deafness (MIDD) is a new sub-type of diabetes and results from an A to G substitution at position 3243 of the mitochondrial tRNA(leu(UUR)) gene. This mutation is also associated with a neurological syndrome (MELAS). Recent studies have screened carefully selected diabetic populations and have reported MIDD prevalence rates ranging from undetectable to 60%. The aim of this work was to determine the importance of this sub-type in clinical practice by screening a routine hospital diabetic population. A total of 1440 patients (IDDM and NIDDM) of North European extraction attending two hospital diabetes services were initially screened by questionnaire. This identified 445 patients with one or more features of MIDD and/or MELAS and these subjects were then genotyped. Two patients were identified with the mutation giving a prevalence rate of 0.13% for the whole study population, and 0.45% for the sample with phenotypic features of MIDD. In conclusion, therefore, the 3243 mutation is associated with the phenotypically distinct MIDD sub-type, but this is rare in the routine hospital diabetic population.

Adult↗
PubMed1997

Childhood size is more strongly related than size at birth to glucose and insulin levels in 10-11-year-old children.

In adults low birthweight and thinness at birth are associated with increased risk of glucose intolerance and non-insulin-dependent diabetes mellitus. We have examined the relations between size at birth (birthweight, thinness at birth) and levels of plasma glucose and serum insulin in children, and compared them with the effects of childhood size. We performed a school-based survey of 10-11-year-old British children (response rate 64%) with measurements made after an overnight fast. One group of children (n = 591) was studied fasting while the other (n = 547) was studied 30 min after a standard oral glucose load (1.75 g/kg). Serum insulin was measured by a highly specific ELISA method. Birthweight was assessed by maternal recall and thinness at birth using birth records. Neither fasting nor post-load glucose levels showed any consistent relationship with birthweight or ponderal index at birth. After adjustment for childhood height and ponderal index, both fasting and post-load insulin levels fell with increasing birthweight. For each kg increase in birthweight, fasting insulin fell by 16.9% (95% confidence limits 7.1-25.8%, p = 0.001) and post-load insulin by 11.6% (95% confidence limits 3.5-19.1%, p = 0.007). However, the proportional change in insulin level for a 1 SD increase in childhood ponderal index was much greater than that for birthweight (27.2% and -8.8%, respectively, for fasting insulin). We conclude that low birthweight is not related to glucose intolerance at 10-11 years, but may be related to the early development of insulin resistance. However, in contemporary children obesity is a stronger determinant of insulin level and insulin resistance than size at birth.

Adult↗
PubMed1997

The effect of portal and peripheral insulin delivery on carbohydrate and lipid metabolism in a miniature pig model of human IDDM.

A pig model of insulin-dependent diabetes was used to examine the importance of the portal-systemic insulin gradient for whole-body metabolic control. Six pigs had jugular vein, portal vein, and carotid artery cannulae implanted before being made diabetic (150 mg kg[-1] streptozotocin). Each animal received 4 weeks of portal and 4 weeks of peripheral insulin delivery in random order. The blood glucose target range was 5-10 mmol x l(-1), and serum fructosamine and fasting and postprandial blood glucose concentrations were not different between peripheral and portal insulin infusion. Insulin requirement was not different between the 4 week infusion periods, but fasting peripheral insulin levels after peripheral delivery (124 +/- 16 (mean +/- SEM) pmol x l[-1]) were significantly higher (p < 0.05) than in portally infused (73.8 +/- 5.4 pmol x l[-1]) or pre-diabetic control animals (68.4 +/- 3.6 pmol x l[-1]). Basal hepatic glucose output was also higher (p < 0.05) in peripherally (4.2 +/- 0.4 mg x kg[-1] x min[-1]) than in portally infused animals (2.9 +/- 0.4 mg x kg[-1] x min[-1]) or controls (3.0 +/- 0.3 mg x kg[-1] x min[-1]). Clamp glucose metabolic clearance rate was, however, not different between the peripheral and portal insulin delivery routes (8.1 +/- 1.0 vs 9.0 +/- 0.7 ml x kg[-1] x min[-1]), although both were significantly lower (p < 0.05) than that measured in prediabetic control animals (11.7 +/- 1.0 ml x kg[-1] x min[-1]). Lipid profiles and subfractions were similar in all three groups. It is concluded that the portal route of delivery is superior to the peripheral in maintaining more appropriate insulin concentrations and control of hepatic glucose output, although in the absence of euglycaemia it is still associated with significant metabolic abnormalities.

Animals↗
PubMed1997

Multiple metabolic abnormalities in normal glucose tolerant relatives of NIDDM families.

Non-diabetic first degree relatives of non-insulin-dependent diabetic (NIDDM) families are at increased risk of developing diabetes mellitus, and have been studied to identify early metabolic abnormalities. Hormone concentrations measured by specific enzyme immunoassays were assessed in non-diabetic relatives of North European extraction, and control subjects with no family history of diabetes were matched for age, sex and ethnicity. A 75-g oral glucose tolerance test was conducted and those with newly diagnosed NIDDM were excluded. Basal insulin resistance was determined by homeostasis model assessment (HOMA), and hepatic insulin clearance by C-peptide:insulin molar ratio. Relatives (n = 150) were heavier (BMI: p < 0.0001) than the control subjects (n = 152), and had an increased prevalence of impaired glucose tolerance (15 vs 3%, p < 0.01). The relatives had increased fasting proinsulin levels and decreased C-peptide levels following the glucose load, while insulin levels were increased at all time points. To examine whether the differences in hormone levels were secondary to the differences in glucose tolerance and adiposity, we studied 100 normal glucose tolerant relatives and control subjects pair-matched for age, sex, waist-hip ratio and BMI. The differences in proinsulin levels were no longer apparent. However, the relatives remained more insulin resistant, and had decreased C-peptide levels and C-peptide:insulin ratios at all time points. In conclusion, we have identified several metabolic abnormalities in the normal glucose tolerant relatives, and propose that the decreased hepatic insulin clearance helps to maintain normoglycaemia in the face of combined insulin resistance and decreased insulin secretion.

Adult↗
PubMed1997

Social inequality in coronary risk: central obesity and the metabolic syndrome. Evidence from the Whitehall II study.

This report describes the social distribution of central obesity and the metabolic syndrome at the Whitehall II study phase 3 examination, and assesses the contribution of health related behaviours to their distribution. Cross-sectional analyses were conducted utilising data collected in 1991-1993 from 4978 men and 2035 women aged 39-63 years who completed an oral glucose tolerance test. There was an inverse social gradient in prevalence of the metabolic syndrome. The odds ratio (95% confidence interval) for having the metabolic syndrome comparing lowest with highest employment grade was: men 2.2 (1.6-2.9), women 2.8 (1.6-4.8). Odds ratios for occupying the top quintile of the following variables, comparing lowest with highest grade, were, for waist-hip ratio: men 2.2 (1.8-2.8), women 1.6 (1.1-2.4); post-load glucose: men 1.4 (1.1-1.8), women 1.8 (1.2-2.6); triglycerides: men 1.6 (1.2-2.0), women 2.2 (1.5-3.3); fibrinogen: men 1.7 (1.4-2.3), women 1.9 (1.2-2.8). Current smoking status, alcohol consumption and exercise level made a small contribution (men 11%, women 9%) to the inverse association between socioeconomic status and metabolic syndrome prevalence. In conclusion, central obesity, components of the metabolic syndrome and plasma fibrinogen are strongly and inversely associated with socioeconomic status. Our findings suggest the metabolic syndrome may contribute to the biological explanation of social inequalities in coronary risk. Health related behaviours appear to account for little of the social patterning of metabolic syndrome prevalence.

Adult↗