150 resultados para Fasting Glucose


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Background: The long-term effects of skipping breakfast on cardiometabolic health are not well understood.

Objective: The objective was to examine longitudinal associations of breakfast skipping in childhood and adulthood with cardiometabolic risk factors in adulthood.

Design:
In 1985, a national sample of 9–15-y-old Australian children reported whether they usually ate breakfast before school. During follow-up in 2004–2006, 2184 participants (26–36 y of age) completed a meal-frequency chart for the previous day. Skipping breakfast was defined as not eating between 0600 and 0900. Participants were classified into 4 groups: skipped breakfast in neither childhood nor adulthood (n = 1359), skipped breakfast only in childhood (n = 224), skipped breakfast only in adulthood (n = 515), and skipped breakfast in both childhood and adulthood (n = 86). Diet quality was assessed, waist circumference was measured, and blood samples were taken after a 12-h fast (n = 1730). Differences in mean waist circumference and blood glucose, insulin, and lipid concentrations were calculated by linear regression.

Results: After adjustment for age, sex, and sociodemographic and lifestyle factors, participants who skipped breakfast in both childhood and adulthood had a larger waist circumference (mean difference: 4.63 cm; 95% CI: 1.72, 7.53 cm) and higher fasting insulin (mean difference: 2.02 mU/L; 95% CI: 0.75, 3.29 mU/L), total cholesterol (mean difference: 0.40 mmol/L; 95% CI: 0.13, 0.68 mmol/L), and LDL cholesterol (mean difference: 0.40 mmol/L; 95% CI: 0.16, 0.64 mmol/L) concentrations than did those who ate breakfast at both time points. Additional adjustments for diet quality and waist circumference attenuated the associations with cardiometabolic variables, but the differences remained significant.

Conclusions: Skipping breakfast over a long period may have detrimental effects on cardiometabolic health. Promoting the benefits of eating breakfast could be a simple and important public health message.

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Introduction and Purpose: Brain-derived neurotrophic factor (BDNF) and physical inactivity contribute to the development of the metabolic syndrome (MetS). There appears to be an association between BDNF and risk factors for MetS, and the effects of resistance training (RT) on BDNF and metabolic risk in middle-aged individuals with high and low numbers of metabolic risk factors (HiMF and LoMF, respectively) are unclear and are the focus of this research.

Methods: Forty-nine men (N = 25) and women (N = 24) aged 50.9 ± 6.2 yr were randomized to four groups, HiMF training (HiMFT), HiMF control (HiMFC), LoMF training (LoMFT), and LoMF control (LoMFC). Before and after 10 wk of RT, participants underwent tests for muscle strength and anthropometry, and a fasting blood sample was taken. Data were analyzed using Spearman correlations and repeated-measures ANOVA.

Results: BDNF was positively correlated with plasma triglycerides, glucose, HbA1C, and insulin resistance. BDNF was elevated in HiMF compared with LoMF (904.9 ± 270.6 vs 709.6 ± 239.8 respectively, P = 0.01). Training increased muscle strength and lean body mass but had no effect on BDNF levels or any examined risk factors.

Conclusion: BDNF levels correlated with risk factors for MetS and were elevated in individuals with HiMF. RT had no effect on BDNF levels or other risk factors for MetS. As RT has an effect on muscle strength and lean body mass, it should be added to other nonpharmacological interventions for middle-aged individuals with HiMF such as aerobic and/or diet.

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For many years the Diabetes Associations of several countries have recommended the dietary elimination of added sucrose. However, contrary to popular belief, there is no evidence that modest use of added sucrose is detrimental to diabetic control. In this study of 17 non-insulin dependent diabetics, the medium-term metabolic effects of the daily supplementation of a subject's usual diet with either 28 g of sucrose or with saccharin and starch of equivalent sweetener and energy value, were compared over six-week periods. Neither dietary period had any significant effect on fasting concentrations of blood glucose, plasma insulin, GIP or serum triglyceride. The metabolic responses to two different test meals, consisting of a standard breakfast supplemented with either sucrose or saccharin plus starch, did not differ significantly either between test meals or between dietary periods. Similarly neither dietary period had any significant effect on urinary excretion of glucose. Na+ or K+. There was no significant difference in mean blood pressure between dietary periods.

The results of this medium-term study indicate that there are no metabolic contraindications to including a moderate amount of sucrose (up to 28 g e 7 teaspoons) in the diets of patients with non-insulin dependent diabetes mellitus.

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This paper describes two complementary bioanalytical experiments for analyzing the concentration of glucose in sports drinks. The first experiment is a spectrophotometric enzyme assay employing the enzymes glucose oxidase (GOx) and horseradish peroxidase (HRP). The glucose is oxidized by the GOx, producing hydrogen peroxide, which is the substrate for HRP. In the reduction of the H2O2 a chromogen is oxidized, causing a color change. In the partner experiment, the GOx is immobilized on a platinum electrode using a dialysis membrane. The hydrogen peroxide produced in the enzyme reaction is monitored amperometrically by oxidizing the hydrogen peroxide produced. The simple method of preparing the enzyme electrode is useful in demonstrating the important parameters in defining the response of enzyme electrodes. The same sports drinks are analyzed in both experiments. The two experiments together illustrate the advantage of bioanalysis in analyzing complex samples with minimal sample preparation.

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An experiment was conducted to measure the effect of diet on circulating concentrations of metabolic hormones and metabolites in cows undergoing extended lactations. Two groups of 6 Holstein-Friesian cows managed for lactations of 670 d were used in the experiment. One group was fully fed on a total mixed ration (TMR), whereas the other group grazed fresh pasture supplemented with grain (P+G). On 7 occasions between 332 and 612 d in milk, concentrations of metabolic hormones and glucose were measured in the blood plasma of each cow. Cows fed TMR gained more weight and body condition than P+G cows, but did not produce more milk during the study period. Only 3 of the TMR cows continued to lactate until 612 d in milk compared with all 6 of the P+G cows. Blood plasma from cows fed TMR had higher concentrations of glucose, insulin, glucagon, insulin-like growth factor 1, and leptin, but lower concentrations of growth hormone, than that from P+G cows. These changes were consistent with the preferential deposition of energy into adipose tissue at the expense of milk production and presumably were induced by a diet that provided precursors for gluconeogenesis that were in excess of the requirements for maintenance and prevailing milk production. The mechanism responsible for some TMR cows putting on excess weight and reducing or ceasing milk production is uncertain, but this observation has important implications for the nutritional management of cows in extended lactation programs.

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Migration to industrialised countries poses a “double whammy” for type 2 diabetes among sub-Saharan African migrant and refugee adults. This population group has been found to be at an increased risk of obesity and type 2 diabetes, which may be further aggravated by inadequate vitamin D status. Thus, this study aimed to describe the demographics of vitamin D insufficiency, obesity, and risk factors for type 2 diabetes among sub-Saharan African migrants and refugees aged 20 years or older living in Melbourne, Australia (n=49). Data were obtained by a questionnaire, medical assessment, and fasting blood samples. The mean serum 25-hydroxyvitamin D level was 27.3 nmol/L (95% CI: 22.2, 32.4 nmol/L); with 25-hydroxyvitamin D levels <50 nmol/L occurring in 88% of participants. Participants displayed a cluster of risk factors for type 2 diabetes and cardiovascular disease: 62% were overweight or obese, 47% had insulin resistance (HOMA-IR ≥2), 25% had low density lipoprotein cholesterol levels ≥3.5 mmol/L, 24.5% had high density lipoprotein cholesterol levels ≤1.03 mmol/L, 34.6% had borderline or high levels of total cholesterol (≥5.2 mmol/L), 18.2% had borderline or high levels of triglyceride (≥1.7 mmol/L), and 16% had hypertension (systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mmHg). These findings suggest that sub-Saharan African migrants and refugees may be at risk of type 2 diabetes and atherosclerosis-related diseases such as ischemic heart disease, stroke, and peripheral vascular disease. Well-designed vitamin D interventions that incorporate lifestyle changes are urgently needed in this sub-population.

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This paper introduces a method of modeling noninvasive glucose sensing for patients who suffer from diabetes mellitus. The proposed technique involves simulation of light propagation through biological tissue with an embedded photonic crystal. The proposed detection technique is Raman spectroscopy and the use of the photonic crystal enables the enhancement of Raman scattering by engineering the photon density of states. Further enhancement can be achieved using noble metal clusters which result in surface enhanced Raman scattering and has the ability to provide enhancements of up to a million times.

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Insulin-regulated aminopeptidase (IRAP), a marker of glucose transporter 4 (GLUT4) storage vesicles (GSVs), is the only protein known to traffic with GLUT4. In the basal state, GSVs are sequestered from the constitutively recycling endosomal system to an insulin-responsive, intracellular pool. Insulin induces a rapid translocation of GSVs to the cell surface from this pool, resulting in the incorporation of IRAP and GLUT4 into the plasma membrane. We sought to identify proteins that interact with IRAP to further understand this GSV trafficking process. This study describes our identification of a novel interaction between the amino terminus of IRAP and the Akt substrate, AS160 (Akt substrate of 160 kDa). The validity of this interaction was confirmed by coimmunoprecipitation of both overexpressed and endogenous proteins. Moreover, confocal microscopy demonstrated colocalization of these proteins. In addition, we demonstrate that the IRAP-binding domain of AS160 falls within its second phosphotyrosine-binding domain and the interaction is not regulated by AS160 phosphorylation. We hypothesize that AS160 is localized to GLUT4-containing vesicles via its interaction with IRAP where it inhibits the activity of Rab substrates in its vicinity, effectively tethering the vesicles intracellularly.

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The renin–angiotensin system (RAS) is functional within adipose tissue and angiotensin II, the active component of RAS, has been implicated in adipose tissue hypertrophy and insulin resistance. In this study, captopril, an angiotensin converting enzyme (ACE) inhibitor that prevents angiotensin II formation, was used to study the development of diet-induced obesity and insulin resistance in obesity prone C57BL/6J mice. The mice were fed a high fat diet (w/w 21% fat) and allowed access to either water or water with captopril added (0.2 mg/ml). Body weight was recorded weekly and water and food intake daily. Glucose tolerance was determined after 11–12 weeks. On completion of the study (after 16 weeks of treatment), the mice were killed and kidney, liver, epididymal fat and extensor digitorum longus muscle (EDL) were weighed. Blood samples were collected and plasma analysed for metabolites and hormones. Captopril treatment decreased body weight in the first 2 weeks of treatment. Food intake of captopril-treated mice was similar to control mice prior to weight loss and was decreased after weight loss. Glucose tolerance was improved in captopril-treated mice. Captopril-treated mice had less epididymal fat than control mice. Relative to body weight, captopril-treated mice had increased EDL weight. Relative to control mice, mice administered captopril had a higher plasma concentration of adiponectin and lower concentrations of leptin and non-esterified fatty acids (NEFA). The results indicate that captopril both induced weight loss and improved insulin sensitivity. Thus, captopril may eventually be used for the treatment of obesity and Type 2 diabetes.

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We investigated the possible association between the sterol regulatory element-binding protein-1c gene (SREBP-1c) rs2297508 polymorphism and the changes in lipid profiles in a high-carbohydrate and low-fat (high-CHO/LF) diet in a Chinese population well characterized by a lower incidence of coronary heart disease and a diet featuring higher carbohydrate and lower fat. Fifty-six healthy youth (aged 22.89 ± 1.80 years) were given wash-out diets of 31% fat and 54% carbohydrate for 7 days, followed by the high-CHO/LF diet of 15% fat and 70% carbohydrate for 6 days, without total energy restriction. Fasting blood samples were collected. Serum variables of lipid and glucose metabolism after the wash-out and high-CHO/LF diets, as well as the rs2297508 polymorphism, were analyzed. Compared with the male subjects on the wash-out diet, significantly elevated levels of high-density lipoprotein cholesterol (HDL-C) and decreased levels of apolipoprotein B-100 were observed in the male carriers of the C allele after the high-CHO/LF diet. In the female subjects, significantly increased triacylglycerol levels, insulin, and homeostasis model assessment of insulin resistance (HOMA-IR) were found in the GG genotype after the high-CHO/LF diet. These results suggest that the C allele of the rs2297508 polymorphism is associated with a retardation of the increases in serum triacylglycerol, serum insulin, and HOMA-IR in females and with the elevated serum HDL-C in males after the high-CHO/LF diet.

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OBJECTIVE To examine whether serum 25-hydroxyvitamin D (25OHD) and dietary calcium predict incident type 2 diabetes and insulin sensitivity.

RESEARCH DESIGN AND METHODS A total of 6,537 of the 11,247 adults evaluated in 1999–2000 in the Australian Diabetes, Obesity and Lifestyle (AusDiab) study, returned for oral glucose tolerance test (OGTT) in 2004–2005. We studied those without diabetes who had complete data at baseline (n = 5,200; mean age 51 years; 55% were women; 92% were Europids). Serum 25OHD and energy-adjusted calcium intake (food frequency questionnaire) were assessed at baseline. Logistic regression was used to evaluate associations between serum 25OHD and dietary calcium on 5-year incidence of diabetes (diagnosed by OGTT) and insulin sensitivity (homeostasis model assessment of insulin sensitivity [HOMA-S]), adjusted for multiple potential confounders, including fasting plasma glucose (FPG).

RESULTS During the 5-year follow-up, 199 incident cases of diabetes were diagnosed. Those who developed diabetes had lower serum 25OHD (mean 58 vs. 65 nmol/L; P < 0.001) and calcium intake (mean 881 vs. 923 mg/day; P = 0.03) compared with those who remained free of diabetes. Each 25 nmol/L increment in serum 25OHD was associated with a 24% reduced risk of diabetes (odds ratio 0.76 [95% CI 0.63–0.92]) after adjusting for age, waist circumference, ethnicity, season, latitude, smoking, physical activity, family history of diabetes, dietary magnesium, hypertension, serum triglycerides, and FPG. Dietary calcium intake was not associated with reduced diabetes risk. Only serum 25OHD was positively and independently associated with HOMA-S at 5 years.

CONCLUSIONS Higher serum 25OHD levels, but not higher dietary calcium, were associated with a significantly reduced risk of diabetes in Australian adult men and women.