Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Body Fat Distribution”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,369 records · Page 76Linked to original sources

Clinical and metabolic presentation of the lipodystrophic syndrome in HIV-infected children.

OBJECTIVE: To investigate body fat distribution and glucose and lipid metabolism in HIV-infected children with the aim of describing the lipodystrophic syndrome in children. DESIGN: Cross-sectional study including 39 HIV-infected children aged 3-18 years. MAIN OUTCOME MEASURES: Clinical lipodystrophy was defined as peripheral fat wasting (facial and/or buttock and/or limb atrophy with arm skinfold thickness lower than the third percentile of the reference values for sex and age) and/or truncal adiposity (breast enlargement and/or buffalo neck and/or relative abdominal obesity with trunk : arm skinfold ratio > 2 standard deviations). Fasting serum lipid concentrations were measured and an oral glucose tolerance test was performed. RESULTS: Of 39 HIV-infected children, lipodystrophy was observed in 13 children (33.3%): eight with truncal lipohypertrophy, three with peripheral lipoatrophy and two with combined lipodystrophy. Combined lipodystrophies were observed only in adolescents with a more severe presentation than in prepubertal children. Lipodystrophic children had higher fasting insulinaemia (7.0+/-8.5 versus 3.0+/-2.3 microU/ml; P = 0.07), suggesting a certain degree of insulin-resistance. Hypercholesterolaemia (23% versus 15%; P = 0.59 ) and hypertriglyceridaemia (15% versus 11%; P = 0.76) were observed with the same proportion in the lipodystrophic as in the non-lipodystrophic groups; 23% of the non-lipodystrophic children had dyslipidaemia. CONCLUSION: The lipodystrophic syndrome prevails in HIV-infected children in the three clinical forms initially described in adults but appears less severe before the initiation of puberty. Insulin-resistance occurs in lipodystrophic children only, whereas dyslipidaemia exists in non-lipodystrophic children as well, suggesting that dyslipidaemia could reflect subclinical alteration of the adipose tissue.

Adolescent↗

Modernity and obesity in coastal and Highland Papua New Guinea.

OBJECTIVE: To investigate the association between individual degree of modernization and obesity in Papua New Guineans using a score of relative 'modernity'. DESIGN: Cross-sectional survey in six populations with varying degrees of modernity. Independent effects of modernity score, components of modernity score, age and physical activity were assessed in relation to general obesity (body mass index (BMI)) and body fat distribution (waist-hip ratio (WHR)). A sub-study of the relationship between diet and modernity was also performed. SETTING: Population-based samples of subjects in three Highland and three coastal locations in the developing country of Papua New Guinea (PNG). SUBJECTS: 1877 subjects > or = 25 years of age attended the survey. MEASUREMENTS: Age, physical activity, BMI, WHR, 2-h oral glucose tolerance test, and modernity score, based on area of origin, father's employment, type and duration of individual's employment, education, years in an urban centre, housing type and spouse score. RESULTS: More modern subjects had higher mean BMI and lower levels of physical activity, and mean WHR also varied with modernity in men but not women. In linear regression analysis, total modernity score was significantly associated with both BMI and WHR in men and women, independently of age and physical activity. When components of the modernity score were examined, younger age, more sophisticated housing and increasing number of years in an urban centre were independently associated with BMI in men and women, while education level and reduced physical activity were also significant predictors in men. Associations with WHR were weaker. Results of the dietary sub-study suggested that the lowest energy and nutrient intakes occurred in the least modern men and women. CONCLUSION: Aspects of modernity, such as more sophisticated housing and greater number of years spent in an urban centre, may be markers of higher income and increasing adoption of Western ways, which in turn are associated with physical inactivity and increased availability of energy-dense Western food, thus promoting obesity in this rapidly developing Pacific nation.

Adult↗

Visceral adipose tissue cutoffs associated with metabolic risk factors for coronary heart disease in women.

OBJECTIVE: This study determined whether there is a critical level of visceral adipose tissue (VAT) associated with elevated coronary heart disease (CHD) risk factors in a cohort of women >45 years of age. RESEARCH DESIGN AND METHODS: Measurements of body composition (dual-energy X-ray absorptiometry), body fat distribution (computed tomography), fasting and 2-h postprandial (75-g) glucose concentrations, and fasting lipoprotein lipid and insulin concentrations were performed in 233 perimenopausal (9%) and postmenopausal women (age 59 +/- 6 years, 79% Caucasian, 16% on hormone replacement therapy). RESULTS: Women in the lowest VAT quintile (< or =105 cm(2)) had higher concentrations of HDL and HDL(2) cholesterol, lower LDL/HDL cholesterol ratios and triglyceride concentrations, and lower fasting glucose and insulin concentrations than women in the remaining four quintiles (P values <0.05-0.001). Women in the second lowest VAT quintile (106-139 cm(2)) had higher HDL and HDL(2) cholesterol and lower LDL/HDL ratios than women with a VAT > or =163 cm(2) (P < 0.05). Logistic regression analyses showed that women with a VAT of 106-162 cm(2) are 2.5 times more likely to have a low HDL cholesterol (P < 0.05), while women with a VAT > or =163 cm(2) are 5.5 times more likely to have a low HDL cholesterol (P < 0.01) and approximately 4.0 times more likely to have a high LDL/HDL ratio (P < 0.05) compared with women with a VAT < or =105 cm(2). Women with a VAT > or =163 cm(2) are at a higher risk of having impaired glucose tolerance (P < 0.01). CONCLUSIONS: A VAT > or =106 cm(2) is associated with an elevated risk, and a VAT > or =163 cm(2) with an even greater risk, for these metabolic CHD risk factors compared with women with a VAT < or =105 cm(2). These values may prove useful for defining "visceral obesity" and for identifying women most likely to benefit from preventative interventions.

Absorptiometry, Photon↗

Sagittal abdominal diameter as a practical predictor of visceral fat.

OBJECTIVE: To evaluate the relationships between the supine sagittal abdominal diameter (SAD) and visceral fat, as well as to evaluate intra- and inter-observer reliability of sagittal diameter measurement. PATIENTS: Twenty-eight women ranging in age from 27-78 y with a body mass index (BMI) ranging from 16.9-48.1 kg/m2 and 23 men ranging in age from 32-75 y with BMI ranging from 20-41.6 kg/m2. MEASUREMENT: Body fat distribution was measured by waist circumference, waist to hip ratio (WHR), SAD, anthropometrically assessed and a single slice of computed tomography (CT) at the L4-L5 level. RESULTS: In both genders, a significant association was found between visceral adipose tissue (AT) and SAD, as evaluated by CT (women r = 0.80; men r = 0.83, P < 0.001), and SAD by anthropometry (women r = 0.76; men r = 0.82, P < 0.001), as well as between visceral AT and waist circumference (women r = 0.76, men r = 0.86, P < 0.001) and WHR (women r = 0.57, P < 0.01, men r = 0.80, P < 0.001). A significant association was also found between subcutaneous AT and SAD by anthropometry (women r = 0.79, men r = 0.74, P < 0.001). After adjusting for BMI, the association between subcutaneous AT and SAD was no longer significant in men and only moderately significant in women (r = 0.42, P < 0.05), while the association between visceral AT and SAD by anthropometry remained significant in both genders (women r = 0.63, P < 0.001; men r = 0.66, P < 0.001). When the subjects were divided into two groups according to BMI (lean to moderately overweight women with BMI < 28 and men with BMI < 30 and obese women with BMI > 28 and men with BMI > 30) we found that the relationships between SAD by anthropometry, as well as SAD by CT and visceral AT, were higher in lean to moderately overweight subjects than in those who were obese. High inter-observer correlation was found concerning SAD measurement (r = 0.99, P < 0.001). Intra- and inter-observer precision as evaluated by coefficient of variation and intraclass correlation coefficient for SAD measurement was very high. CONCLUSION: Our study shows the usefulness of SAD by anthropometry to predict visceral fat and its very high inter- and intra-observer precision.

Abdomen↗

Disturbances in insulin secretion and sensitivity in women with the polycystic ovary syndrome.

Insulin resistance, defined as a diminished effect of a given dose of insulin on glucose homeostasis, is a highly prevalent feature of women with PCOS. Insulin resistance in PCOS is closely associated with an increase in truncal-abdominal fat mass, elevated free fatty acid levels, increased androgens, particularly free testosterone through reduced SHBG levels, and anovulation. The causes for insulin resistance in PCOS are still unknown. One line of evidence suggests that an increase in truncal-abdominal fat mass and subsequently increased free fatty acid levels induce insulin resistance in women with PCOS. Increased effects of corticosteroids and a relative reduction in oestrogen and progesterone seem to be involved in the aberrant body fat distribution. Conversely, there are also results supporting primary, genetic target cell defects as a cause of insulin resistance in PCOS. An explanation for these seemingly contradictory results could be that the group of women with PCOS is heterogeneous with respect to the primary event in carbohydrate/insulin disturbances. Also insulin secretion in PCOS is characterized by heterogeneity. At one end of the spectrum is a large subgroup of mainly obese women with reduced insulin secretion, which appears to result from failure of the beta cells to compensate for insulin resistance in susceptible women, resulting in glucose intolerance and NIDDM. In the insulin-resistant patients with normal glucose tolerance, most of the hyperinsulinaemia is probably due to secondarily increased insulin secretion and decreased insulin degradation. However, a component of the increased first-phase insulin release is not due to measurable insulin resistance. Notably, this is also found in lean women with normal insulin sensitivity, and is not reversed after weight reduction, in contrast to the findings for insulin resistance. The implications of this enhanced insulin release are not fully clear, but it may tentatively be associated with carbohydrate craving and subsequently increased risks for development of obesity and insulin resistance. It may represent a primary disturbance of insulin secretion in PCOS or may be associated with the perturbed steroid balance in anovulation. The insulin-androgen connection in PCOS appears to be amplified by several different mechanisms, notably in both directions, the initiating event probably varying between individuals. Thus insulin increases the biological availability of potent steroids, primarily testosterone, through the suppression of SHBG synthesis. Insulin is also involved as a progonadotrophin in ovarian steroidogenesis, with the possible net result of interfering with ovulation and/or increasing ovarian androgen production in states of hyperinsulinaemia. Conversely, testosterone may indirectly contribute to insulin resistance through facilitating free fatty acid release from abdominal fat, but perhaps also through direct muscular effects at higher serum levels. It seems likely that this constitution, presumably genetic, would provide evolutionary advantages in times of limited nutrition, given the energy-saving effects of insulin resistance. Hypothetically, hyperinsulinaemia (primary) could provide a stimulus to ensure intake of nourishment, but unlimited food supplies could in some cases initiate a vicious 'anabolic' circle, in which several of the proposed amplifying mechanisms between insulin and androgens--in both directions--could take part.

Adipose Tissue↗

A strategy for arterial risk assessment and management in type 2 (non-insulin-dependent) diabetes mellitus. European Arterial Risk Policy Group on behalf of the International Diabetes Federation European Region.

People with Type 2 (non-insulin-dependent) diabetes mellitus die mainly from cardiovascular and cerebrovascular disease. Furthermore, the major burden of their symptoms arise from arterial disease, including peripheral vascular disease. However, management guidelines for Type 2 diabetes continue to focus on blood glucose control, which is only one of a number of arterial risk factors found with this type of diabetes. Clinically it is evident that blood glucose control continues to occupy centre-stage in the management of Type 2 diabetes as practised by many physicians. Even when arterial risk factors such as smoking or raised serum triglycerides are noted, their management is often relatively neglected. As part of the St Vincent Declaration Action Programme, a working group has sought consensus on the number and relative importance of arterial risk factors requiring management in quality diabetes care. The group seeks to assist those devising protocols and guidelines, records and quality systems, and those charged with directly advising and educating people with diabetes. Arterial risk factors that can be routinely identified and monitored, and modified by application of management protocols, include high blood pressure, high serum total and LDL cholesterol, low serum HDL cholesterol and raised serum triglycerides, poor blood glucose control, smoking, high body mass index and body fat distribution. Aspirin can modify hypercoagulability, but this is not easily monitored. Arterial risk factors that cannot be modified, but which have an impact on the intensity of management of other factors, include ethnic group, gender, and family history of arterial disease. Raised albumin excretion is an arterial risk factor and can be modified, but it is not clear whether this reduces cardiovascular risk. For many of the risk factors, levels of high, medium, and low risk can be set. These can be used, in consultation with the patient, to determine appropriate interventions and provide feedback on risk reduction resulting from successful management.

Cardiovascular Diseases↗

Anthropometric data indicate nutritional homogeneity in Hadza foragers of Tanzania.

We analyzed body mass index (BMI = wt/height(2)) and percent body fat (BF%) in adults of the Hadza, an egalitarian society with a strong food-sharing ethic, to examine variation in energetic status in relation to sex, age, and time of year. Data collected from 26 camps over six field seasons gave a cross-sectional sample of 238 males and 235 females and a small longitudinal sample (n = 54). We found that mean BMI showed no sex difference [20.1 +/- 1.6 (SD) kg/m(2) for males and 20.3 +/- 2.2 kg/m(2) for females] and remained similar, regardless of age or time of year. Mean BF% showed a significant sex difference, as expected [10.6 +/- 3.2 (SD) % for males and 19.0 +/- 7.0% for females (P < 0.0001)], with two significant age departures from uniformity: (1) males in the prime age group (30-45 years, n = 79) had a higher mean BF% (11.7%) compared to other ages (P < 0.03), and (2) females in the extreme elderly age group (> 75 years, n = 11) had a lower mean BF% (11.3%) compared to other ages (P < 0.004). In the longitudinal sample, we found no significant change over time in mean BMI or BF%. However, relative change in BF% fluctuated within individuals by as much as 20% of initial values for both sexes. Taken collectively, our results support the idea of broad nutritional homogeneity among the Hadza, but indicate that subtle, potentially important differences in energetic condition exist as well.

Adipose Tissue↗

Personal and non-occupational risk factors and occupational injury/illness.

BACKGROUND: The materials handling industry performs is an essential function in the world economy, however, it is plagued with occupationally related injuries and illnesses. Understanding the risk factors may assist this industry in alleviating these injuries and illnesses, as well as their associated costs. METHODS: Forty-eight personal and non-occupational risk factors were measured and evaluated for statistically significant relationships with occupational injury in 442 volunteer manual material handlers who worked for three different companies, at nine US locations, with 15 different job descriptions. OSHA 200 logs were used to ascertain evidence of occupational injury within this population for 1 year after the testing and measurement was completed. RESULTS: Higher occurrences of injury were significantly associated with six risk factors in the univariate model (odds ratios 1.51-4.00). The significantly (P < 0.05) related risk factors in the univariate model were aerobic power, smoking status, perceived fitness level, fishing/hunting as a hobby, speed limit obeyance, and witnessing or being involved in a violent fight. In the multivariate analysis, five risk factors (aerobic power, smoking status, percent body fat, body mass index, and sit-and-reach measured flexibility) were significantly (P < 0.05) associated with occupational injury. Odds ratios in the multivariate analysis varied from 1.42 to 10.11. CONCLUSION: Evidence of an association of occupational injury occurrence with certain risk factors presented in personal and non-occupational univariate and multivariate models is shown. In industry, effective injury reduction programs should go beyond traditional methods of job-related ergonomic risk factors and include personal factors such as smoking, weight control, and alcohol abuse.

Adult↗

Prospective study of adiposity and weight change in relation to prostate cancer incidence and mortality.

BACKGROUND: Adiposity has been linked inconsistently with prostate cancer, and few studies have evaluated whether such associations vary by disease aggressiveness. METHODS: The authors prospectively examined body mass index (BMI) and adult weight change in relation to prostate cancer incidence and mortality in 287,760 men ages 50 years to 71 years at enrollment (1995-1996) in the National Institutes of Health-AARP Diet and Health Study. At baseline, participants completed questionnaires regarding height, weight, and cancer screening practices, including digital rectal examinations and prostate-specific antigen tests. Cox regression analysis was used to calculate relative risks (RR) and 95% confidence intervals (95% CIs). RESULTS: In total, 9986 incident prostate cancers were identified during 5 years of follow-up, and 173 prostate cancer deaths were ascertained during 6 years of follow-up. In multivariate models, higher baseline BMI was associated with significantly reduced total prostate cancer incidence, largely because of the relationship with localized tumors (for men in the highest BMI category [>or=40 kg/m(2)] vs men in the lowest BMI category [<25 kg/m(2)]: RR, 0.67; 95% CI, 0.50-0.89; P = .0006). Conversely, a significant elevation in prostate cancer mortality was observed at higher BMI levels (BMI <25 kg/m(2): RR, 1.0 [referent group]; BMI 25-29.9 kg/m(2): RR, 1.25; 95% CI, 0.87-1.80; BMI 30-34.9 kg/m(2): RR, 1.46; 95% CI, 0.92-2.33; and BMI >or=35 kg/m(2): RR, 2.12; 95% CI, 1.08-4.15; P = .02). Adult weight gain from age 18 years to baseline also was associated positively with fatal prostate cancer (P = .009), but not with incident disease. CONCLUSIONS: Although adiposity was not related positively to prostate cancer incidence, higher BMI and adult weight gain increased the risk of dying from prostate cancer.

Adiposity↗

Epidemiologic and genetic follow-up study of 544 Minnesota breast cancer families: design and methods.

In 1944, a case-control family study was initiated at the Dight Institute for Human Genetics at the University of Minnesota to study the influences of childbearing breastfeeding, and hereditary susceptibility on the occurrence and age-of-onset of breast cancer. Index cases (probands) were women ascertained at the Tumor Clinic of the University of Minnesota Hospital. Medical history and life style information were obtained on probands and relatives, and all cancers were histologically verified. A total of 544 families were studied, with probands diagnosed between 1931 and 1952. All of the records and pathology slides have been maintained from the original study; for most probands this includes the original tissue blocks. We are conducting a historical cohort study of selected of selected first- and second-degree female relatives (sisters, daughters, nieces, granddaughters) of the probands and a group of control women identified as the spouses of all male first- and second-degree relatives (brothers, sons, grandsons, and nephews). The subsequent development of breast cancer is being determined to quantify the absolute risk associated with a positive family history. Current disease status is ascertained with mammography, and stromal density is measured using digital imaging. Segregation analysis will be applied to examine how non-genetic factors such as diet, exogenous hormone use, and body fat distribution influence risk in women at high risk because of family history. A subset of families are being selected for molecular analysis of the BRCA1 gene or for linkage analyses to identify putative susceptibility loci other than BRCA1. Documented cancer histories were known for at least three generations, and the current study extends the pedigrees up to four or five generations for every family, allowing a detailed description of familial risk. This cohort study of breast cancer families is likely to be important in both quantity and quality of data and will serve as a major genetic epidemiologic resource, being free of selection bias and having relevant non-genetic exposure determined in at least four generations.

Adult↗

Insulin resistance and breast-cancer risk.

Life-style has a major influence on the incidence of breast cancer. To evaluate the effects of life-style related metabolic-endocrine factors on breast cancer risk we conducted a case-control study comparing 223 women aged 38 to 75 years presenting with operable (stage I or II) breast cancer and 441 women of the same age having no breast cancer, who participated in a population-based breast cancer screening program. Women reporting diabetes mellitus were excluded. Sera from 110 women of the same age group presenting with early stage melanoma, lymphoma or cervical cancer were used as a second 'other-cancer control group'. Serum levels of C-peptide were significantly higher in early breast cancer cases compared to controls. The same was found for the ratios C-peptide to glucose or C-peptide to fructosamine, indicating insulin resistance. Sex hormone binding globulin was inversely, triglycerides and available estradiol were positively related to C-peptide. Serum C-peptide levels were related to body mass index (BMI), and to waist/hip ratio (WHR), in particular in controls. However, the relative increase of C-peptide, C-peptide to glucose or C-peptide to fructosamine in cases was independent of BMI or WHR. The log relative risk was linearly related to the log C-peptide levels. Relative risk according to quintiles, and adjusted for age, family history, BMI and WHR, for women at the 80% level was 2.9 as compared with those at the 20% level for C-peptide. Elevated C-peptide or C-peptide to fructosamine values were not observed in the sera from women belonging to the 'other-cancer control group'. This study suggests that hyperinsulinemia with insulin resistance is a significant risk factor for breast cancer independent of general adiposity or body fat distribution.

Adult↗

Insulin-like growth-factor-binding protein 3 is decreased in early-stage operable pre-menopausal breast cancer.

Insulin-like growth factor I (IGF-I) is a potent mitogen for human breast-cancer cells in vitro. In circulation, most of IGF-I is bound to IGF-binding protein 3 (IGFBP-3). This high-affinity binding is thought to have an important limiting effect on the availability of IGF-I for biological activity. To assess the availability of IGF-I for receptor binding, we determined serum levels of IGF-I and IGFBP-3 and IGF-I/IGFBP-3 ratios. In a case-control study, 150 women aged 38 to 75 years presenting with stage-I or -II breast cancer were investigated just prior to surgery (n = 76), or to irradiation one month after surgery (n = 74). The population-based control group consisted of 441 women of the same age having no breast cancer. Women reporting diabetes mellitus or other hormonal abnormalities were excluded. Premenopausal cases showed elevated IGF-I serum concentrations, decreased IGFBP-3 levels and increased IGF-I/IGFBP-3 ratios. The IGF-I/IGFBP-3 ratio was a significant breast-cancer risk factor, also after adjustment for age, family history, height, body-mass index, body-fat distribution, and serum levels of C-peptide. The relative risk was 7.34 for the highest compared with the lowest quintile of IGF-I/IGFBP-3. The presence or absence of tumor had no influence on these results. Increased levels of available IGF-I in the circulation of pre-menopausal women may contribute to the development of breast cancer.

Adult↗

Human immunodeficiency virus genotype and hypertriglyceridemia.

Many HIV patients develop a progressive syndrome of abnormal body fat distribution accompanied by hypertriglyceridemia. Antiretroviral agents are thought to be etiologic in the syndrome, often termed "highly active antiretroviral therapy (HAART)-associated lipodystrophy." In the course of clinical HIV genotype testing, we observed that our HIV patients with hypertriglyceridemia had viral genotypes that were more highly mutated than those of our therapy-matched control patients. Hypertriglyceridemia was statistically associated with predicted resistance for three nucleoside reverse transcriptase inhibitors: zidovudine, abacavir, and stavudine. Statistical analysis of 51 patients in retrospect revealed a strong association of mutations at reverse transcriptase codons M41 and T215 with hypertriglyceridemia (chi-square (chi(2)) = 8.375, P=.0038; and chi(2)=7.445, P=.0064, respectively). This was in contrast to silent mutations, which occurred at equivalent rates in retroviral genotypes of patients with and without hypertriglyceridemia. The findings imply that the HIV genotype itself may be a significant etiologic factor in antiretroviral-associated lipodystrophy.

Adult↗

Effects of health information in youth and young adulthood on risk factors for chronic diseases--20-year study results from the Amsterdam Growth and Health Longitudinal Study.

In the Amsterdam Growth and Health Longitudinal Study (AGAHLS) biological risk factors for chronic diseases were measured on eight separate occasions over a period of 20 years in a group of apparently healthy males and females (n = 164). Data were first collected from participants at 13 years of age. At each of the eight measurements, a medical checkup was performed and participants were given information about their current health status based on their personal biological risk factor profile (cholesterol, blood pressure, body composition, and physical fitness). A comparable group (n = 113) was measured on two occasions only: at age 13 and again at age 33. It was hypothesized that the group with eight measurements would present a more favorable 20-year development of the risk factors than the group with only two measurements. In the present article the six additional measurements with personal feedback of one's health status were perceived as an "intervention," even though the AGAHLS never intended to improve the lifestyle or health of its subjects. The intervention appeared to have had a positive effect on body fat distribution and, in men, on systolic blood pressure. However, it was expected that these significant results were not true effects of the intervention, but that they were type-I errors. For the other variables, total cholesterol, high-density lipoprotein cholesterol, and the ratio between these two, for the sum of four skinfolds, diastolic blood pressure, neuromotor fitness, and for maximal oxygen uptake, the 20-year development did not differ between the two groups. Thus, the effects of a 20-year health measurement and information intervention begun in youth on biologic risk factors for chronic diseases were limited. The absence of clear significant findings may be due to the low contrast between the two groups, as only six intervention measurements were conducted over a period of 20 years. Another reason may be that the young and relatively healthy population under study here was not amenable to changing their fitness and health.

Adolescent↗

A preponderance of small dense LDL is associated with specific insulin, proinsulin and the components of the insulin resistance syndrome in non-diabetic subjects.

Recently, the presence of small dense low density lipoprotein (LDL) has been postulated to be a stronger risk factor for coronary heart disease than large LDL. While small dense LDL has been associated with individual components of the insulin resistance syndrome such as hypertension, high triglyceride level, low high density (HDL) cholesterol, and diabetes mellitus, there has been little work exploring whether LDL size is decreased in subjects with multiple metabolic disorders. We examined the association of LDL size and pattern to specific insulin (which does not cross-react with proinsulin), proinsulin, increased triglyceride, decreased HDL, hypertension and impaired glucose tolerance in 488 non-diabetic subjects from the San Antonio Heart Study. LDL size was significantly related to specific insulin, proinsulin and the fasting proinsulin/insulin ratio. Small dense LDL was significantly associated with high triglyceride level, decreased HDL cholesterol, hypertension and impaired glucose tolerance. LDL size (A) decreased in a stepwise fashion with increasing number of the metabolic disorders described above (zero 262.6 +/- 9.4; one 257.0 +/- 9.3; two 256.4 +/- 9.4; three 249.0 +/- 9.1; and four 244.9 +/- 9.0). These results were similar in men and women and in non-Hispanic whites and Mexican Americans. The association between LDL size and the number of metabolic disorders remained statistically significant even after adjustment for obesity, body fat distribution, gender, ethnicity, proinsulin and insulin concentrations. Furthermore, decreases in LDL size are also significantly associated with both a selective beta-cell defect (as estimated by the fasting proinsulin/insulin ratio) and insulin resistance (as estimated by the fasting insulin concentrations) although the association was somewhat stronger for the latter. We conclude that small dense LDL may form part of the insulin resistance syndrome in non-diabetic subjects.

Diabetes Mellitus↗

Birthweight and adult health outcomes in a biethnic population in the USA.

Recent data indicate that low-birthweight adults are at a higher risk than their high-birthweight peers of developing ischemic heart disease or a cluster of conditions known as the IRS, which includes dyslipidaemias, hypertension, unfavorable body fat distribution and NIDDM. Thus far these observations have been limited to Caucasians from the United Kingdom. we extended these observations to a broader segment of the general population by studying the association of birthweight and adult health outcomes in a biethnic population of the United States. We divided a group of 564 young adult Mexican-American and non-Hispanic white men and women participants of the San Antonio Heart Study into tertiles of birthweight and compared metabolic, anthropometric, haemodynamic, and demographic characteristics across these tertile categories. Additionally, we studied birthweight as a predictor of the clustering of diseases associated with the IRS, defined as any two or more of the following conditions: hypertension, NIDDM or impaired glucose tolerance, dyslipidaemia. Normotensive, non-diabetic individuals whose birthweight was in the lowest tertile had significantly higher levels of fasting serum insulin and a more truncal fat deposition pattern than individuals whose birthweight was in the highest tertile, independently of sex, ethnicity, and current socioeconomic status. Also, the odds of expressing the IRS increased 1.72 times (95% confidence interval: 1.16-2.55) for each tertile decrease in birthweight. These findings were independent of sex, ethnicity, and current levels of socioeconomic status or obesity. In conclusion, low birthweight could be a major independent risk factor for the development of adult chronic conditions commonly associated with insulin resistance in the general population.

Adult↗

Relationship of glucose intolerance to coronary risk in Afro-Caribbeans compared with Europeans.

Afro-Caribbeans have low mortality rates from coronary heart disease, despite a high prevalence of diabetes mellitus. We examined 1166 Afro-Caribbean and European men and women aged 40-64 years in a community survey in London, UK. Prevalence of glucose intolerance (combining impaired glucose tolerance, new and known diabetes) was 31% in Afro-Caribbeans and 14% in Europeans (p < 0.001). In men, the prevalence of probable coronary heart disease was 6% in Afro-Caribbeans and 13% in Europeans (p < 0.01). Triglyceride was lower in Afro-Caribbeans than Europeans; in men, HDL cholesterol was higher. Afro-Caribbean men were less centrally obese, while Afro-Caribbean women were more centrally obese than their European counterparts. Fasting and 2-h insulin levels were higher in Afro-Caribbeans than Europeans. Glucose intolerance was associated with high triglyceride, low HDL cholesterol and central obesity in European but not in Afro-Caribbean men. In Europeans, fasting triglyceride was 1.49 mmol/l in normoglycaemic and 1.89 mmol/l in glucose intolerant men (p < 0.05), in Afro-Caribbean men triglyceride was 1.08 and 1.22 mmol/l, respectively. Waist hip ratio was 0.94 in normoglycaemic, and 0.98 in glucose intolerant European men (p < 0.001). In Afro-Caribbean men, waist hip ratio was 0.93 in both groups. At each level of insulin, glucose or central obesity, triglyceride was lower in Afro-Caribbean men and women than in Europeans. We speculate that despite high insulin levels, Afro-Caribbeans have a favourable lipoprotein pattern which persists in the presence of glucose intolerance, and may be related to body fat distribution.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Resistin levels are normal in hypothyroidism and remain unchanged after attainment of euthyroidism: relationship with insulin levels and anthropometric parameters.

The aim of this controlled prospective study was to investigate resistin levels in hypothyroidism before and after restoration of euthyroidism and correlate the results with body weight (BW), body fat (BF), waist circumference (WC), body mass index (BMI) and serum insulin levels. Fifty-three hypothyroid patients with Hashimoto's disease (6 males, 47 females) and 30 controls matched for age, BMI and BF were investigated. Anthropometric parameters, resistin and insulin levels were measured. All patients were started on levothyroxine treatment and 4 to 5 months after initiation of treatment the investigations were repeated. Hypothyroid patients exhibited normal resistin values, which were no different from controls (mean+/-SD 7.4+/-4.0 vs 5.1+/-3.5 ng/ml, p=0.063). Normalization of circulating thyroid hormone levels produced no significant change in resistin levels (7.4+/-4.0 vs 6.8+/-4.2 ng/ml, p=ns) and post-treatment resistin levels did not differ from euthyroid controls. Furthermore, no gender difference was demonstrated in resistin levels either before (6.4+/-3.7 for males vs 7.6+/-4.1 ng/ml for females, p=ns) or after therapy (7.9+/-4.3 vs 6.7+/-4.3 ng/ml, for males and females respectively, p=ns), nor was there a difference in resistin levels in either sex induced by treatment of hypothyroidism (6.4+/-3.7 vs 7.9+/-4.3 ng/ml for males, p=ns, and 7.6+/-4.1 vs 6.7+/-4.3 ng/ml for females, p=ns). However, a small but significant difference in resistin levels was found between female patients and female controls (7.6+/-4.1 vs 5.0+/-4.0 ng/ml, p=0.047). Insulin levels and homeostasis model assessment insulin resistance (HOMA-IR) index did not differ before and after treatment in hypothyroid patients (13.0+/-10.2 vs 12.6+/-11.8 microU/ml, 22.7+/-1.4 vs 21.8+/-1.3, respectively, p=ns for both) or between patients and controls. In conclusion, our results demonstrate that resistin levels are normal in hypothyroidism and remain within normal range after attainment of euthyroidism. Resistin is not associated with serum insulin and HOMA-IR index, as well as BMI, BF, WC and BW.

Adolescent↗