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Lipoprotein(a) [Lp(a)] contributes to cardiovascular disease risk. A genetically determined size polymorphism in apolipoprotein(a) [apo(a)], determined by the number of Kringle (K) repeats, inversely regulates Lp(a) levels. Nongenetic factors including dietary saturated fat influence Lp(a) levels. However, less is known about the effects of carbohydrates including dietary sugars. In this double-blind, parallel arm study among 32 overweight/obese adults, we investigated the effect of consuming glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks on Lp(a) level and assessed the role of the apo(a) size polymorphism. The mean (±SD) age of participants was 54 ± 8 years, 50% were women, and 75% were of European descent. Following the 10-week intervention, Lp(a) level was reduced by an average (±SEM) of -13.2% ± 4.3% in all participants (P = 0.005); -15.3% ± 7.8% in the 15 participants who consumed glucose (P = 0.07); and -11.3% ± 4.5% in the 17 participants who consumed fructose (P = 0.02), without any significant difference in the effect between the two sugar groups. Relative changes in Lp(a) levels were similar across subgroups of lower versus higher baseline Lp(a) level or carrier versus noncarrier of an atherogenic small (≤22K) apo(a) size. In contrast, LDL-C increased. In conclusion, in older, overweight/obese adults, consuming sugar-sweetened beverages reduced Lp(a) levels by ∼13% independently of apo(a) size variability and the type of sugar consumed. The Lp(a) response was opposite to that of LDL-C and triglyceride concentrations. These findings suggest that metabolic pathways might impact Lp(a) levels., Competing Interests: Conflict of interest The authors declare that they have no conflicts of interest with the contents of this article., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Background & Aims: Accumulation of visceral adipose tissue is associated with insulin resistance and cardio-vascular disease. The aim of this study was to elucidate whether removal of a large amount of visceral fat by omentectomy in conjunction with Roux en-Y gastric bypass operation (RYGB) results in enhanced improvement of insulin sensitivity compared to gastric bypass surgery alone., Methods: Eighty-one obese women scheduled for RYGB were included in the study. They were randomized to RYGB or RYGB in conjunction with omentectomy. Insulin sensitivity was measured by hyperinsulinemic euglycemic clamp before operation and sixty-two women were also reexamined 2 years post-operatively. The primary outcome measure was insulin sensitivity and secondary outcome measures included cardio-metabolic risk factors., Results: Two-year weight loss was profound but unaffected by omentectomy. Before intervention, there were no clinical or metabolic differences between the two groups. The difference in primary outcome measure, insulin sensitivity, was not significant between the non-omentectomy (6.7 ± 1.6 mg/kg body weight/minute) and omentectomy groups (6.6 ± 1.5 mg/kg body weight/minute) after 2 years. Nor did any of the cardio-metabolic risk factors that were secondary outcome measures differ significantly., Conclusion: Addition of omentectomy to gastric bypass operation does not give an incremental effect on long term insulin sensitivity or cardio-metabolic risk factors. The clinical usefulness of omentectomy in addition to gastric bypass operation is highly questionable., Clinical Trial Registration Number: NCT01785134., (Copyright © 2014 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.)

Objective: To assess how change in sleep duration is related to subsequent obesity., Methods: In this 10-year follow-up, 4903 non-pregnant participants answered a questionnaire on sleeping habits, obesity, and lifestyle factors (questions identical to baseline questionnaire). Habitual normal sleepers were defined as sleeping 6-9 h/night at both baseline and follow-up, whereas women sleeping <6 h/night or ≥9 h/night at both occasions were defined as habitual short sleepers and habitual long sleepers, respectively. Logistic regression was used to analyze associations between changes in sleep duration, general obesity (body mass index ≥30 kg/m(2)), weight gain (≥10 kg) and also, central obesity (waist circumference ≥88 cm), and increase in waist circumference (≥10 cm) at follow-up., Results: Among younger women (aged <40 years) both habitual short sleepers and habitual long sleepers had a higher prevalence of general (short: 31.3%, P < 0.0001; long: 38.1%, P = 0.01) and central obesity (short: 60.5%, P = 0.01; long: 82.4%, P = 0.01) compared with habitual normal sleepers (general obesity: 8.9%; central obesity: 35.9%) at follow-up. Younger women who were short sleepers at baseline but normal sleepers at the follow-up had a higher prevalence of both general (19.3%, P = 0.01) and central obesity (45.4%, P = 0.07) compared with habitual normal sleepers at follow-up. In adjusted analyses, both habitual short [adjusted odds ratio (aOR), 6.78; 95% confidence interval (CI), 2.71-17.0] and long (aOR, 4.64; 95% CI, 1.09-19.8) sleep durations were risk factors for general obesity in younger women. In younger women habitual long sleep duration was a risk factor also for central obesity (aOR, 6.05; 95% CI, 1.19-30.7) whereas habitual short sleep duration was not (aOR, 1.93; 95% CI, 0.87-4.81). Similar results were seen also for weight gain and increased waist circumference as dependent variables. In addition, decreased sleep duration from normal to short duration was a risk factor for both weight gain (aOR, 1.85; 95% CI, 1.14-3.02) and increased waist circumference (aOR, 1.84; 95% CI, 1.20-2.81). There were no associations between changes in sleep duration and any of the measures of obesity at the follow-up in women aged >40 years at baseline., Conclusion: In younger women, both habitual short and long sleep duration was a risk factor for obesity, whereas no such relationship was seen in older women., (Copyright © 2014 Elsevier B.V. All rights reserved.)

A marked increase in the frequency of obesity at the population level has resulted in an increasing number of obese women entering pregnancy. The increasing realization of the importance of the fetal environment in relation to chronic disease across the lifespan has focused attention on the role of maternal obesity in fetal development. Previous studies have demonstrated that obesity during adolescence and adulthood can be traced back to fetal and early childhood exposures. This review focuses on factors that contribute to early developmental events, such as epigenetic modifications, the potential for an increase in inflammatory burden, early developmental programming changes such as the variable development of white versus brown adipose tissue, and alterations in organ ontogeny. We hypothesize that these mechanisms promote an unfavorable fetal environment and can have a long-standing impact, with early manifestations of chronic disease that can result in an increased demand for future health care. In order to identify appropriate preventive measures, attention needs to be placed both on reducing maternal obesity as well as understanding the molecular, cellular, and epigenetic mechanisms that may be responsible for the prenatal onset of chronic disease.

Objective: To assess characteristics of short sleepers and long sleepers and to assess association between sleep duration and central obesity in a population-based sample of women., Method: Non-pregnant women ≥20 years that were randomly selected from the population-registry of Uppsala, Sweden, answered a questionnaire (n=6461) including questions on sleeping habits and somatic disorders., Results: There was a U-shaped association between sleep duration and waist circumference. Short sleeping women (<5 h) had a waist circumference of 89.2±14.9 cm (mean±SD) decreasing to 82.9±11.9 cm for women sleeping 7-<8 h and increasing to 89.0±16.7 cm for women sleeping ≥10 h. Both short sleepers and long sleepers were more often physically inactive, smokers, ill or taking medication, and psychologically distressed than normal sleepers (6-<9 h). In women <50 years both short and long sleep duration were risk factors for central obesity. Short sleep duration remained a risk factor for central obesity, whereas the association with long sleep duration did not reach statistical significance after adjustments., Conclusions: Short sleepers and long sleepers showed differences in characteristics compared to normal sleepers. Furthermore, we showed an independent association between short sleep duration and central obesity, which was strongest in younger women. It is important to identify short sleepers, especially in younger women., (Copyright © 2012 Elsevier B.V. All rights reserved.)

Background/objectives: The results of short-term studies in humans suggest that, compared with glucose, acute consumption of fructose leads to increased postprandial energy expenditure and carbohydrate oxidation and decreased postprandial fat oxidation. The objective of this study was to determine the potential effects of increased fructose consumption compared with isocaloric glucose consumption on substrate utilization and energy expenditure following sustained consumption and under energy-balanced conditions., Subjects/methods: As part of a parallel arm study, overweight/obese male and female subjects, 40-72 years, consumed glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks. Energy expenditure and substrate utilization were assessed using indirect calorimetry at baseline and during the 10th week of intervention., Results: Consumption of fructose, but not glucose, led to significant decreases of net postprandial fat oxidation and significant increases of net postprandial carbohydrate oxidation (P<0.0001 for both). Resting energy expenditure (REE) decreased significantly from baseline values in subjects consuming fructose (P=0.031) but not in those consuming glucose., Conclusions: Increased consumption of fructose for 10 weeks leads to marked changes of postprandial substrate utilization including a significant reduction of net fat oxidation. In addition, we report that REE is reduced compared with baseline values in subjects consuming fructose-sweetened beverages for 10 weeks.

Context: Results from animal studies suggest that consumption of large amounts of fructose can promote inflammation and impair fibrinolysis. Data describing the effects of fructose consumption on circulating levels of proinflammatory and prothrombotic markers in humans are unavailable., Objective: Our objective was to determine the effects of 10 wk of dietary fructose or glucose consumption on plasma concentrations of monocyte chemoattractant protein-1 (MCP-1), plasminogen activator inhibitor-1 (PAI-1), E-selectin, intercellular adhesion molecule-1, C-reactive protein, and IL-6., Design and Setting: This was a parallel-arm study with two inpatient phases (2 wk baseline, final 2 wk intervention), conducted in a clinical research facility, and an outpatient phase (8 wk) during which subjects resided at home., Participants: Participants were older (40-72 yr), overweight/obese (body mass index = 25-35 kg/m(2)) men (n = 16) and women (n = 15)., Interventions: Participants consumed glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 wk. Blood samples were collected at baseline and during the 10th week of intervention., Main Outcome Measures: Fasting concentrations of MCP-1 (P = 0.009), PAI-1 (P = 0.002), and E-selectin (P = 0.048) as well as postprandial concentrations of PAI-1 (P < 0.0001) increased in subjects consuming fructose but not in those consuming glucose. Fasting levels of C-reactive protein, IL-6, and intercellular adhesion molecule-1 were not changed in either group., Conclusions: Consumption of fructose for 10 wk leads to increases of MCP-1, PAI-1, and E-selectin. These findings suggest the possibility that fructose may contribute to the development of the metabolic syndrome via effects on proinflammatory and prothrombotic mediators.

Purpose of Review: To review the current scientific literature and recent clinical trials on HIV protease inhibitors and their potential role in the pathogenesis of lipodystrophy and metabolic disorders., Recent Findings: HIV protease inhibitor treatment may affect the normal stimulatory effect of insulin on glucose and fat storage. Further, chronic inflammation from HIV infection and protease inhibitor treatment trigger cellular homeostatic stress responses with adverse effects on intermediary metabolism. The physiologic outcome is such that total adipocyte storage capacity is decreased, and the remaining adipocytes resist further fat storage. This process leads to a pathologic cycle of lipodystrophy and lipotoxicity, a proatherogenic lipid profile, and a clinical phenotype of increased central body fat distribution similar to the metabolic syndrome., Summary: Protease inhibitors are a key component of antiretroviral therapy and have dramatically improved the life expectancy of HIV-infected individuals. However, they are also associated with abnormalities in glucose/lipid metabolism and body fat distribution. Further studies are needed to better define the pathogenesis of protease inhibitor-associated metabolic and body fat changes and their potential treatment.

Objective: The aim of this study was to explore the outcome and the problems of drop-out in the treatment of obese outpatients at an academic obesity unit., Design: A two-year clinical treatment evaluation., Subjects: A total of 117 obese subjects, 83 women and 34 men, mean aged 50 (23-70) years, with an average body mass index (BMI) of 39.0 kg/m2 (28.8- 64.7)., Intervention: All treatment was based on group therapy and included behaviour modification and nutrition counselling. A team of nurses, dieticians, a physiotherapist, a psychotherapist and a physician supervised the treatment. Two programmes were used. Group 1 initially received a low-calorie diet (LCD) for seven weeks combined with the behaviour treatment programme. Group 2 was treated with the behaviour treatment programme only. All subjects were offered complementary treatment according to their medical needs., Results: There was a continuous drop-out of subjects during the two-year treatment period with an overall drop-out rate of 53%. Anthropometric characteristics, medical history or reasons for drop-out had no impact on the drop-out rate. In completers the weight reduction after two years was 9.2 [+/-10.8 standard deviation (S.D.) kg. In non-completers the weight reduction of the last observed weight measurement was 4.7 (+/-7.9 S.D.) kg. After year two, the weight reduction in Group 1 was 8.8 (+/-12.2 S.D.) kg, and in Group 2 was 9.7 (+/-8.0 S.D.) kg., Conclusion: This study has showed the difficulties of long-term clinical treatment of obese outpatients, even in a specialised obesity clinic. The findings demonstrate that educated and experienced staff together with an extended package of treatment options is not enough to keep patients in treatment for two years. However though the drop-out rate was high, two thirds of the included subjects reduced their weight, which is a satisfactory result in a clinical setting. The drop-out rate and the reasons for dropping out could give a clue in which direction the diagnostics and analysis of the subject's individual needs in health care should be directed.

The objective of this study was to explore whether there were differences in organisational setting and professional intervention between health professionals who, after 1 year of education, and ongoing supervision for all together 30 months, started obesity treatment and those who did not. Furthermore to analyse what factors facilitate the start of obesity treatment. One hundred and seventy-one health professionals from different parts of Sweden were included in the education. One hundred and thirty-five health professionals remained in the study for up to 2.5 years. Eighty-seven subjects started the obesity treatment program, whereas 48 subjects had no possibility to start treatment. Significantly more of those who started the behavioural treatment program had previous theoretical education and clinical experience of obesity. They also, to a greater degree, had a go-ahead from the management and support from physicians, colleagues and were more likely to be part of a team or had a colleague to work with. In addition, they could find the time to organise and plan the treatment. Supervision had a significant positive influence on starting up the treatment program. Education, working organization, a structural behavioural treatment program, seems to be significant factors in facilitating and increasing the likelihood for a start.

Objective: This study evaluates the association between abdominal obesity and the intake of dairy fat and calcium using information from dietary data and the relative content of the fatty acids 14:0, 15:0, and 17 : 0 in serum phospholipids (PL) and adipose tissue (AT), which are suggested biological markers for dairy fat intake. This study also explores how the associations were affected when under-reporters (URs) were separated from the analyses., Design: Cross-sectional study., Subjects: In all, 301 healthy 63-y-old men with different degrees of fasting-insulin concentrations., Methods: Sagittal abdominal obesity (SAD), dietary intake assessed by a 7-day food registration, and the fatty acid composition in serum PL and AT were measured. URs (n=88) and non-under-reporters (non-URs, n=213) were identified by Goldberg's equation, which compares energy intake with energy expenditure, both expressed as multiples of the basal metabolic rate., Results: The intake of dairy fat, expressed as g/100 g fat, was inversely correlated with SAD; however, this association was only observed in the URs (r=-0.36, P=0.001) and not in the non-URs (r=-0.04, P=0.59). The intake of calcium was inversely correlated with SAD in both groups, although the association was weaker in the non-URs. The intake of dairy fat was related to the relative content of the fatty acids 14:0, 15:0, and 17 : 0 in serum PL and AT (r ranging between 0.32 and 0.55). When these fatty acids were correlated to SAD, inverse associations were seen except for 14:0 in PL (r ranging between -0.17 and -0.29., Conclusion: If there is a true inverse association between the intake of dairy fat and SAD, it remains to explain why this association was not seen in the non-URs. The data gave some indications of an inverse association between SAD and the intake of calcium. The diverse findings observed when the URs and non-URs were separated highlight the question of how to use and interpret dietary data in URs when diet-disease relationships are investigated.

Objective: It is clinically important to find noninvasive markers of insulin resistance and hyperproinsulinemia because they both predict cardiovascular and diabetes risk. Sagittal abdominal diameter (SAD) or "supine abdominal height" is a simple anthropometric measure previously shown to predict mortality in men, but its association with insulin resistance and hyperproinsulinemia is unknown., Research Design and Methods: In a common high-risk group of 59 moderately obese men (aged 35-65 years, BMI 32.6 +/- 2.3 kg/m(2)), we determined anthropometry (SAD, BMI, waist girth, and waist-to-hip ratio [WHR]); insulin sensitivity (euglycemic-hyperinsulinemic clamp); and plasma concentrations of intact proinsulin, specific insulin, C-peptide, glucose, and serum IGF binding protein-1 (IGFBP-1). To compare SAD with other anthropometric measures, univariate and multiple regression analyses were used to determine correlations between anthropometric and metabolic variables., Results: SAD showed stronger correlations to all measured metabolic variables, including insulin sensitivity, than BMI, waist girth, and WHR. SAD explained the largest degree of variation in insulin sensitivity (R(2) = 0.38, P < 0.0001) compared with other anthropometric measures. In multiple regression analyses, including all anthropometric measures, SAD was the only independent anthropometric predictor of insulin resistance (P < 0.001) and hyperproinsulinemia (P < 0.001)., Conclusions: In obese men, SAD seems to be a better correlate of insulin resistance and hyperproinsulinemia (i.e., cardiovascular risk) than other anthropometric measures. In overweight and obese individuals, SAD could represent a simple, cheap, and noninvasive tool that could identify the most insulin resistant in both the clinic and clinical trials evaluating insulin sensitizers. These results need confirmation in larger studies that also include women and lean subjects.

Objective: To compare two group treatment programmes for obese outpatients. Both programmes included behaviour modification, nutrition counselling, very-low-calorie diet (VLCD) and a continuous measuring of metabolic and anthropometrical status, but they differed regarding the treatment intensiveness. The main aim was to study whether intensive treatment gives a larger weight reduction compared with less intensive treatment and what level of input from health care personnel is needed to reach adequate treatment results., Design: A 2-y randomised clinical trial., Subjects: A total of 43 obese subjects aged 24-60 y, BMI 35 kg/m(2) (29-48)., Intervention: Two programmes were used. Both were based on group therapy and were supervised by a dietitian and a psychologist. Group 1 received a continuous intensive treatment with planned group meetings every fortnight during the first year and six group meetings the second year. Group 2 had planned group meetings every third month. Anthropometrical and metabolic data were measured every third month in both groups. The VLCD periods were the same., Results: There was no evidence that a more intensive treatment promotes a larger weight reduction. Weight reduction after 1 y: group 1, -7.6 (+/-0.97) kg, BMI -2.6 (+/-0.3) kg/m(2); group 2, -6.4 (+/-1.16) kg, BMI -2.2 (+/-0.4) kg/m(2). Weight reduction after 2 y: group 1, -6.8 (+/-1.4) kg, BMI -2.4 (+/-0.3) kg/m(2); group 2, -8.6 (+/-1.6) kg, BMI -3.0 (+/-0.3) kg/m(2). The dropout rate was 26%., Conclusion: There were no significant differences in weight reduction, compliance or dropout rate between the groups and there was no evidence that a more intensive treatment promotes a larger weight reduction. This observation is of value when setting up treatment programmes. To measure the metabolic and anthropometrical status during the treatment and to give continuous feedback to the subjects seem to be important factors for compliance. Both treatment programmes gave highly significant weight reductions in the range of 5-10%, which has been referred to as a realistic goal for the treatment of obese patients.

Background: Abdominal obesity is strongly related to metabolic disorders. Recent research suggests that dietary conjugated linoleic acid (CLA) reduces body fat and may improve metabolic variables in animals. The metabolic effects of CLA in abdominally obese humans have not yet been tested., Objective: To investigate the short-term effect of CLA on abdominal fat and cardiovascular risk factors in middle-aged men with metabolic disorders., Methods: Twenty-five abdominally obese men (waist-to-hip ratio (WHR), 1.05+/-0.05; body mass index (BMI), 32+/-2.7 kg/m(2) (mean+/-s.d.)) who were between 39 and 64-y-old participated in a double-blind randomised controlled trial for 4 weeks. Fourteen men received 4.2 g CLA/day and 10 men received a placebo. The main endpoints were differences between the two groups in sagittal abdominal diameter (SAD), serum cholesterol, low-density lipoprotein, high-density lipoprotein, triglycerides, free fatty acids, glucose and insulin., Results: At baseline, there were no significant differences between groups in anthropometric or metabolic variables. After 4 weeks there was a significant decrease in SAD (cm) in the CLA group compared to placebo (P=0.04, 95% CI; -1.12, -0.02). Other measurements of anthropometry or metabolism showed no significant differences between the groups., Conclusions: These results indicate that CLA supplementation for 4 weeks in obese men with the metabolic syndrome may decrease abdominal fat, without concomitant effects on overall obesity or other cardiovascular risk factors. Because of the limited sample size, the effects of CLA in abdominal obesity need to be further investigated in larger trials with longer duration.

Higher plasma fibrinogen levels are associated with increased risk of myocardial infarction in adults, but little is known about factors that influence fibrinogen levels in childhood. The authors examined the associations of measures of obesity, presence of the (G-455-->A) allele in the beta-fibrinogen promoter gene, and family history of early onset of ischemic heart disease with plasma fibrinogen levels in children. Children (n = 299) were recruited during 1994-1997 from 276 families living in a racially mixed area of New York City. The mean age of the study children was 9.9 years; 79% were Hispanic. The frequency of the (G-455-->A) allele was lower in Hispanics than in non-Hispanic Whites (15.5% vs. 28.3% in children (p < 0.01) and 13.9% vs. 28.3% in parents (p < 0.001)). Graded relations of children's plasma fibrinogen levels were found with tertiles of body mass index (weight (kg)/height (m)2) and sum of skinfolds (tests for linear trend: p < 0.001). Plasma fibrinogen levels in the children were not related to race/ethnicity, presence of the (G-455-->A) allele, or family history. Multiple linear regression analyses adjusting plasma fibrinogen levels for age, sex, race/ethnicity, the (G-455-->A) allele, and family history of early onset of heart disease showed a significant association with either body mass index or sum of skinfolds (p < 0.001 for both models) but not with the other variables.

Objectives: To clarify the type of fetal growth impairment associated with increased blood pressure in adult life, and to establish whether this association is influenced by obesity and is mediated through impairment of insulin action., Design: Cross sectional survey with retrospective ascertainment of size at birth from obstetric archives., Subjects: 1333 men resident in Uppsala, Sweden, who took part in a 1970 study of coronary risk factors at age 50 and for whom birth weight was traced., Main Outcome Measures: Systolic and diastolic blood pressure at age 50., Results: In the full study population for a 1000g increase in birth weight there was a small change in systolic blood pressure of -2.2mmHg (95% confidence interval -4.2 to - 0.3mmHg) and in diastolic blood pressure of -1.0mmHg (-2.2 to 0.1mmHg). Much stronger effects were observed among men who were born at term and were in the top third of body mass index at age 50, for whom a 1000g increase in birth weight was associated with a change of -9.1mmHg (-16.4 to-1.9mmHg) systolic and -4.2mmHg (-8.3 to -0.1mmHg) diastolic blood pressure. Men who were light at birth (<3250g) but were above median adult height had particularly high blood pressure. Adjustment for insulin concentrations reduced the associations of birth weight with systolic and diastolic blood pressure., Conclusions: A failure to realise growth potential in utero (as indicated by being light at birth but tall as an adult) is associated with raised adult blood pressure. Impaired fetal growth may lead to substantial increases in adult blood pressure among only those who become obese. Metabolic disturbances, possibly related to insulin resistance, may provide a pathway through which fetal growth affects blood pressure.

At the 2008 Olympics, the body weight of the athletes varied from 28 to 181 kg and many Olympic athletes therefore today have a stature far from the ancient Greek athletic ideals. Athletes and sports associated with leanness and their medical problems have been researched extensively. However, there has been less focus on those athletes, who may gain a competitive advantage by having excess body fat, being large or oversized. The present review introduces for the first time the concept of Adipositas athletica and gives a description and classification of these athletes. Adipositas athletica is defined as having a higher than 'athletic normal' (Greek Olympic ideals) fat mass and being an elite athlete. The condition is divided into subgroups based on the intent or non-intent to increase body fat per se. Another factor is the intent to increase body mass as well as increasing physiological factors such as strength or endurance. It is concluded that most of the sports-medicine community-physicians, researchers and nutritionists - has neglected these oversized and obese athletes, their long- and short-term morbidity and mortality, their eating problems and the use of performance-enhancing drugs. Although some data on overweight and obese athletes exist, the most remarkable finding when reviewing the literature is the paucity of data. Many unanswered questions remain and great strides remain to be made. [ABSTRACT FROM AUTHOR]

Aims/hypothesis: We examined whether the Pro12-Ala polymorphism of the human peroxisome proliferator-activated receptor-γ2 (PPAR-γ2) gene was related to altered insulin sensitivity among glucose-tolerant subjects or a lower accumulated incidence or prevalence of IGT and Type II (non-insulin-dependent) diabetes mellitus among Scandinavian Caucasians. Methods: The Pro12Ala polymorphism was examined using PCR-RFLP. Whole-body insulin sensitivity measured under hyperinsulinaemic-euglycaemic conditions was estimated in a population-based sample of 616 glucose tolerant Swedish Caucasian men at age 70. In addition, insulin sensitivity index was measured using IVGTT and Bergman minimal modelling in a population-based sample of 364 young healthy Danish Caucasians. Finally, we evaluated whether the polymorphism predicted Type II diabetes and IGT in 841 seventy-year-old Swedish men. A case-control study was carried out in 654 unrelated Danish Type II diabetic patients and 742 Danish glucose tolerant subjects matched for age and sex. Results: Whole-body insulin sensitivity was significantly improved in carriers compared with non-carriers of the Ala-allele of the codon 12 polymorphism in Swedish Caucasian men (6.0 ± 2.5 vs 5.6 ± 2.5 mg · kg–1· min–1· [mU/l]–1· 100, p = 0.044). The same tendency, but not significant, was observed in the insulin sensitivity index among the group of young healthy Danish Caucasians. The incidence of Type II diabetes and IGT among the Swedish subjects at the age of 70 was similar in the three genotype-groups of the Pro12Ala variant and the Ala-allele was not related to a lower prevalence of Type II diabetes in Danish Caucasians. Conclusion/interpretation: The Ala-allele of the PPAR-γ2 polymorphism is associated with improved whole body insulin sensitivity among Swedish Caucasians. [Diabetologia (2001) 44: 1170–1176] [ABSTRACT FROM AUTHOR]

OBJECTIVE: To estimate the reliability of anthropometric measurements in overweight and lean subjects, and to examine the influence of this reliability on correlations to other variables, since low reliability leads to underestimation of correlations. DESIGN: Replicate measurements by two observers in 26 overweight and 25 lean subjects measured at two occasions. MEASUREMENTS: Sagittal abdominal diameter (SAD), waist circumference (waist), waist-to-hip ratio (W/H) and skinfold measurements. RESULTS: Intra-class correlation coefficients (ICCs) for SAD and waist were higher than for W/H (0.98 vs 0.90, P<0.001, and 0.97 vs 0.90, P=0.001, respectively). For waist, the ICC was lower for overweight than for lean subjects (0.85 vs 0.95, P=0.030), but the ICC values were comparable for SAD and W/H (0.92 vs 0.95 and 0.78 vs 0.83, respectively). Intra-observer variations (IOV) for SAD and waist were lower than for W/H (coefficients of variation; 1.6%, 1.4% and 2.3%, respectively), as were intra-subject variations (ISV) (2.7%, 3.0% and 3.4%, respectively). ICC values ranged from 0.84 to 0.93 and were lower for overweight than for lean subjects for biceps, subscapular and umbilical skinfolds (P=0.031, P<0.001 and P=0.048, respectively). Coefficients of variations for skinfold measurements ranged between 7.3% and 16.0% for IOV and between 14.9% and 20.8% for ISV. CONCLUSIONS: The low ICC values imply that correlations can be underestimated in overweight groups. We propose that, because of their higher reliability, SAD and waist have a higher predictive capacity for cardiovascular risk than W/H. SAD is the only measurement with high reliability in both weight groups and its use is recommended. [ABSTRACT FROM AUTHOR]