Insulin sensitivity of blood glucose versus insulin sensitivity of blood free fatty acids in normal, obese, and obese-diabetic subjects

Belfiore, Francesco; Iannello, Silvia; Camuto, Massimo; Fagone, Saverio; Cavaleri, Antonina

doi:10.1053/meta.2001.22518

Cited by 40 publications

(42 citation statements)

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“…In addition, analysis of BMI as a quantitative trait revealed no association with K121Q genotype (Table 3). No evidence of an impact of the variant on measures of insulin sensitivity indices [39][40][41] was observed. In fact, the impact of the gene variant on insulin resistance has been ambiguous, yielding association in some but not all populations studied [16,[19][20][21][22]42].…”

Section: Discussionmentioning

confidence: 88%

Studies of the relationship between the ENPP1 K121Q polymorphism and type 2 diabetes, insulin resistance and obesity in 7,333 Danish white subjects

et al. 2006

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Aims/hypothesis Plasma cell membrane glycoprotein 1 (PC-1) inhibits insulin signalling by direct interaction with the insulin receptor α subunit. This inhibition is enhanced by the minor Q allele of the K121Q polymorphism (rs1044498) in the gene (ENPP1) encoding PC-1. This polymorphism has been studied in relation to insulin resistance, type 2 diabetes and obesity in several populations with conflicting results. We assessed the impact of the ENPP1 K121Q polymorphism on type 2 diabetes, obesity and quantitative metabolic traits in 7,333 Danes. Subjects and methods The K121Q polymorphism was genotyped in the population-based Inter99 study cohort (5,961 subjects) and in a group of 1,386 patients with type 2 diabetes. All subjects were Danish whites.Results No significant associations with type 2 diabetes or related quantitative metabolic traits, including measures of insulin resistance, were detected. However, a meta-analysis of the present and published studies revealed an association with type 2 diabetes (odds ratio per Q allele, 1.17 [95% CI 1.10-1.25], p=1×10 −6 ). In case-control studies comparing subjects of different BMI strata, we observed a putative association of the codon 121 QQ genotype with being overweight (BMI>25 kg/m 2 ; odds ratio 1.63 [95% CI 1.09-2.46], p=0.015), an association not observed when comparing other levels of BMI or when analysing BMI as a quantitative trait. Conclusions/interpretation In a meta-analysis, the ENPP1 codon 121 Q allele associates with type 2 diabetes. However, a similar association was not found in the present study of Danish white subjects. The effect of this variant on obesity in Danish subjects is contentious and further study is needed.

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Section: Discussionmentioning

confidence: 88%

Studies of the relationship between the ENPP1 K121Q polymorphism and type 2 diabetes, insulin resistance and obesity in 7,333 Danish white subjects

et al. 2006

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“…However, the Figure 3 (a) Relation between insulin response to the test meal (expressed as 6-h AUC) and plasma leptin concentrations at 6 h following consumption of a high-fat, mixed meal after 3 days on a low-carbohydrate diet (Low-CHO, r ¼ 0.84, P ¼ 0.009), after 3 days on a high-carbohydrate diet (High-CHO, r ¼ 0.77, P ¼ 0.02) and after 3 days on the same high-carbohydrate diet with 60 min daily of moderate intensity exercise (High-CHO-Ex, r ¼ 0.89, P ¼ 0.003). (b) Relation between whole-body insulin sensitivity (ISI(gly)) (calculated from postprandial insulin and glucose responses 17 ) and plasma leptin concentrations at 6 h following consumption of a high-fat, mixed meal after 3 days on a low-carbohydrate diet (Low-CHO, r ¼ À0.80, P ¼ 0.01), after 3 days on a high-carbohydrate diet (High-CHO, r ¼ À0.75, P ¼ 0.03) and after 3 days on the same high-carbohydrate diet with 60 min daily of moderate intensity exercise (High-CHO-Ex, r ¼ À0.78, P ¼ 0.02).…”

Section: Discussionmentioning

confidence: 99%

“…17 Two-way ANOVA for repeated measures was used to assess the effect of the interventions, postprandial time (0-6 h) and their interaction (intervention Â time). In addition, summary measures of the postprandial insulin and glucose responses were calculated as the total area under serum or plasma concentration vs time curves (AUC) using the trapezoidal rule.…”

Section: Calculations and Statisticsmentioning

confidence: 99%

Plasma leptin is influenced by diet composition and exercise

et al. 2003

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OBJECTIVE: A low-fat, high-carbohydrate diet (r30% of total energy intake as fat) in conjunction with moderate intensity physical activity is widely recommended for weight maintenance and reduction. The aim of this study was to assess the effect of adding daily exercise to a short-term high-carbohydrate diet on fasting and postprandial leptin levels. SUBJECTS: Eight healthy, postmenopausal women aged 6074 y (mean7s.d.) (body mass index, BMI: 26.472.3 kg m À2 ; predicted maximal oxygen uptake: 2972 ml kg À1 min À1 ). DESIGN: Plasma responses were studied after subjects consumed the same high-fat, mixed meal on three occasions: after 3 days on a low-carbohydrate diet (35, 50 and 15% energy from carbohydrate, fat and protein, respectively) (Low-CHO); after 3 days on an isoenergetic high-carbohydrate diet (corresponding values 70, 15 and 15%) (High-CHO); and after 3 days on the same high-carbohydrate diet with 60 min of brisk walking daily (High-CHO-Ex). MEASUREMENTS: Fasting and postprandial plasma or serum concentrations of leptin, glucose and insulin. RESULTS: Fasting leptin was significantly higher (Po0.05) after the High-CHO (18.472.6 ng ml À1 ) (mean7s.e.m.) than after both the Low-CHO and the High-CHO-Ex interventions, which did not differ significantly from each other (16.972.1 and 15.572.0 ng ml À1 , respectively; P ¼ 0.08). Overall (fasted and postprandial states), plasma leptin concentrations were significantly higher after the High-CHO than after the High-CHO-Ex intervention. There was a strong, positive, linear relation between postprandial insulin responses and postprandial leptin concentrations at 6 h. In addition, there was a strong, negative, linear relation between whole-body insulin sensitivity (based on postprandial responses of glucose and insulin) and postprandial leptin concentrations at 6 h. CONCLUSION: Daily moderate intensity exercise, without concomitant changes in body fat mass, suppressed fasting and postprandial circulating leptin concentrations after consumption of a short-term high-carbohydrate diet. As shown in previous studies, insulin appears to be an important modulator of leptinaemia.

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“…A meta-analysis of data from di¡erent studies showed a signi¢cant correlation between ISI-gly and measurements of insulin sensitivity made by the hyperinsulinaemic euglycaemic clamp technique. 41 The index is calculated as follows:…”

Section: Oral Glucose Tolerance Testmentioning

confidence: 99%