The influence of high carbohydrate diet on plasma glucose and insulin of trained subjects

In previous studies we have shown that when endurance athletes refrain from daily exercise for three days, they rapidly loose their enhanced insulin sensitivity. This finding suggests that a precompetitive high carbohydrate diet with reduced training might alter plasma glucose and insulin regulation. To test this hypothesis, six long distance runners were recruited to participate in a five-day experiment. During the first two days, the subjects fasted while running 16 km d-1. Thereafter, they consumed 16.3 MJ (3900 kcal) and 539 g carbohydrate per day for three days while remaining inactive. Before and after each portion of this experiment, an intravenous glucose tolerance test (IVGTT) was performed in fasting state. As expected, fasting with exercise induced a considerable deterioration of glucose tolerance, as reflected by lower K value and higher total area glucose during IVGTT. The high carbohydrate refeeding restored glucose tolerance to a level comparable to that observed when subjects maintain their usual life habits. However, while a decrease in insulin sensitivity is observed in subjects inactive for three days, the insulin sparing effect of exercise training is retained if this period of inactivity is preceded by two days of fast accompanied by exercise. These results show that glucose disposal and insulin response to glucose injection are not adversely modified by the precompetitive "glycogen loading" procedure.     

Glucose tolerance in young and older athletes and sedentary men

Groups of endurance-trained masters athletes (60 +/- 2 yr), older untrained men (62 +/- 1 yr), lean older untrained men (61 +/- 2 yr), endurance-trained young athletes (26 +/- 1 yr), and young untrained men (28 +/- 1 yr) were studied to obtain information on the separate effects of age, physical activity, and body fatness on glucose tolerance and insulin sensitivity. Each subject underwent an oral 100-g glucose tolerance test. Skinfold thickness was determined at six sites. The trained groups had a higher maximum O2 uptake capacity and lower sum of skinfolds than their sedentary peers. The lean older untrained group had a sum of skinfolds similar to that of the young untrained group. The masters athletes, young athletes, and young untrained men exhibited similar glucose tolerance whereas the two older untrained groups had an almost twofold greater total area under the glucose curve (P less than 0.05). The masters and young athletes had significantly blunted plasma insulin responses compared with the other three groups (P less than 0.05). The young and the lean older untrained groups had similar plasma insulin responses with significantly lower insulin levels than the older untrained group (P less than 0.05). These results provide evidence that regularly performed vigorous exercise can, in some individuals, prevent the deterioration of glucose tolerance and insulin sensitivity with age.     

Changes in insulin sensitivity precede changes in body composition during 14 days of step reduction combined with overfeeding in healthy young men

A lifestyle characterized by inactivity and a high-calorie diet is a known risk factor for impaired insulin sensitivity and development of Type 2 diabetes mellitus. To investigate possible links, nine young healthy men (24 ± 3 yr; body mass index of 21.6 ± 2.5 kg/m(2)) completed 14 days of step reduction (10,000 to 1,500 steps/day) and overfeeding (+50% kcal). Body composition (dual X-ray absorptiometry, MRI), aerobic fitness (maximal O(2) consumption), systemic inflammation and insulin sensitivity [oral glucose tolerance test (OGTT), hyperinsulinemic euglycemic clamp] were assessed before (day 0), during (days 3 and 7), and immediately after the intervention (day 14), with follow-up tests (day 30). Body weight had increased at days 7 and 14 (P < 0.05). The amount of visceral fat had increased at day 14 compared with day 0 (P < 0.05). The insulin response to the OGTT had increased at days 7 and 14 (P < 0.05). Insulin sensitivity, estimated using the Matsuda index, had decreased at days 3 and 7 (P < 0.01). At day 14, glucose infusion rates had decreased by ～44% during the euglycemic clamps (P < 0.05). Also, plasma levels of leptin and adiponectin had increased (P < 0.05), whereas no changes were seen in inflammatory markers. At day 30, body weight and whole body adiposity were still elevated compared with day 0 (P < 0.05), whereas the insulin sensitivity as well as the insulin response to the OGTT did not differ from baseline. The glucose response to the OGTT was only affected at day 30, with a decrease compared with day 0. Our data show that insulin sensitivity was impaired after 3 days of inactivity and overfeeding. Impairments in insulin sensitivity occurred before changes in body composition, supporting the notion that the initial steps in impairment of insulin sensitivity may be linked directly to the effects of inactivity and a high calorie intake.     

Contribution of the exercise-induced increment in glucose storage to the increased insulin sensitivity of endurance athletes

The present study was designed to evaluate the contribution of the exercise-induced increment in glucose storage to the increased insulin sensitivity characterizing endurance athletes. Plasma glucose and insulin were measured during an oral glucose tolerance test (OGTT) in six endurance athletes. Glucose storage and lipid oxidation during this test were also determined using indirect calorimetry. These measurements were compared to those obtained in five non-trained subjects who were tested before and during the three days following a 90-min cycle ergometer exercise performed at 69% of their VO2max. As expected, preexercise values of non-trained subjects revealed a much higher insulin response to glucose, and a lower glucose storage and lipid oxidation compared to results obtained in endurance trained individuals. Glucose tolerance was comparable in both groups. The morning following the exercise test, i.e. about 16 h after exercise, glucose storage was significantly increased in non-trained subjects to a level similar to that found in trained subjects. Surprisingly, this was accompanied by higher values of glucose during the OGTT without significant changes in insulinaemia. This impairment in glucose homeostasis was transitory since glucose tolerance had returned to control level on day 2 after exercise. At that time, the increase in glucose storage was less pronounced than in day 1. On day 3 after exercise, glucose and insulin responses to glucose were similar to preexercise values. These results indicate that the increase in glucose storage by acute exercise is not systematically associated with an improved glucose homeostasis, suggesting that other adaptive mechanisms also contribute to the improvement of insulin sensitivity in endurance athletes.     

Plasma insulin and C-peptide responses to oral glucose load after physical exercise in men with normal and impaired glucose tolerance

Blood glucose, plasma insulin and C-peptide responses to oral glucose tolerance test (OGTT) were studied under basal conditions and immediately after 90-min exercise (60% VO2 max) in nondiabetic subjects with normal or impaired glucose tolerance. During the postexercise recovery blood glucose response to OGTT was increased in normal subjects and markedly decreased in those with impaired glucose tolerance, while insulin and C-peptide responses were diminished in both subgroups. The ratio of blood glucose to insulin was similarly elevated in all subjects. Comparing with basal conditions no significant changes were found in C-peptide to insulin ratio in response to OGTT after exercise, although a tendency towards an elevation of this ratio was noted in the subjects with impaired glucose tolerance. The data indicate that the reduced insulin response to OGTT during postexercise recovery in healthy subjects is due to diminished insulin secretion without any substantial changes in the hormone removal from blood, whereas in the glucose intolerant men the latter process may be enhanced.     

Insulin and glucose responses during bed rest with isotonic and isometric exercise

The effects of daily intensive isotonic (68% maximum oxygen uptake (VO2 max)) and isometric (21% maximum extension force) leg exercise on plasma insulin and glucose responses to an oral glucose tolerance test (OGTT) during 14-day bed-rest (BR) periods were investigated in seven young healthy men. The OGTT was given during ambulatory control and on day 10 of the no-exercise, isotonic, and isometric exercise BR periods during the 15-wk study. The subjects were placed on a controlled diet (mean +/- SD = 344 +/- 34 g CHO/day and 3,073 +/- 155 (SD) kcal/day) starting 10 days before each BR period. During BR, basal plasma glucose concentration remained unchanged with no exercise, but increased (P less than 0.05) to 87-89 mg/100 ml with both exercise regimens on day 2, and then fell slightly below control levels on day 13. The fall of glucose content (-11 to -15%) during BR was independent of the exercise regimen and was an adjustment for the loss of plasma vol. The intensity of the response of insulin and glucose to the OGTT (integrated area under the curves) was inversely proportional to the total daily energy expenditure during BR; i.e., the largest response with no exercise, then isometric, isotonic, and ambulatory exercise. It was estimated that at least 1,020 kcal/day must be provided by supplemental exercise to restore the hyperinsulinemia to control levels.     

Effect of resistance exercise on dehydroepiandrosterone sulfate concentrations during a 72-h recovery: relation to glucose tolerance and insulin response

Serum dehydroepiandrosterone sulfate (DHEA-S) concentration is known to be associated with the whole-body insulin sensitivity. The main purpose of the study was to investigate the effect of resistance exercise on DHEA-S concentration during a 72 h post-exercise recovery, and its relation to glucose tolerance and insulin sensitivity. Morning fasted serum samples was obtained from 19 male volunteers (aged 21.1+/-0.4 years) 24 h before the onset of exercise and 24 h, 48 h, and 72 h following exercise for measurements of DHEA-S, cortisol, and TNF-alpha. Oral glucose tolerance test (OGTT) and insulin response were determined 24 h before and 48 h after exercise. We found that resistance exercise causes a delayed suppression in serum DHEA-S levels during recovery (48 h and 72 h). This exercise challenge did not affect glucose tolerance, but insulin response during OGTT was significantly elevated. The increased insulin level was not associated with serum levels of cortisol and TNF-alpha. In conclusion, the present study found that resistance exercise has a DHEA-S lowering effect that persisted for 72 h. This change could be related to the elevated insulin concentrations during OGTT.     

Does age, sex, or ACE genotype affect glucose and insulin responses to strength training?

The purpose of the present study was to determine whether age, sex, or angiotensin I-converting enzyme (ACE) genotype influences the effects of strength training (ST) on glucose homeostasis. Nineteen sedentary young (age = 20-30 yr) men (n = 10) and women (n = 9) were studied and compared with 21 sedentary older (age = 65-75 yr) men (n = 12) and women (n = 9) before and after a 6-mo total body ST program. Fasting insulin concentrations were reduced in young men and in older men with ST (P < 0.05 in both). In addition, total insulin area under the curve decreased by 21% in young men (P < 0.05), and there was a trend for a decrease (11%) in older men (P = 0.06). No improvements in insulin responses were observed in young or older women. The ACE deletion/deletion genotype group had the lowest fasting insulin and insulin areas under the oral glucose tolerance test (OGTT) curve before training (all P < 0.05), but those with at least one insertion allele had a trend for a greater reduction in total insulin area than deletion homozygotes (P = 0.07). These results indicate that ST has a more favorable effect on insulin response to an OGTT in men than in women and offer some support for the hypothesis that ACE genotype may influence insulin responses to ST.     

Endogenous opiate modulators of insulin secretion in the obese

The effects of endogenous opiates on insulin response to oral glucose load were studied in obese subjects and in lean healthy volunteers. None of these having a family diabetes. After 3 days on an 1,800 cal./m2, 40% carbohydrate diet all subjects underwent two standard 75 g oral glucose tolerance tests (OGTT), one of which was accompanied by an i. v. administration of 10 mg of, an antagonist of opiates, the naloxone. In one group of obese impaired oral glucose tolerance test occurred. All obese, but not the lean healthy volunteers, showed: 1) increased basal plasma insulin levels, 2) higher insulin response to OGTT, 3) a decrease in insulin response to OGTT after naloxone administration, with significant differences at 60 min (p less than 0.01) and 90 min (p less than 0.025). In none of the subjects significant differences were observed in blood glucose levels after OGTT plus naloxone administration. These data suggest that increased endogenous opiates may affect insulin response to glucose in obese with impaired or normal oral glucose tolerance test. At present there seems to be no satisfactory explanation for unchanged blood glucose levels during OGTT with and without naloxone despite a decrease in insulin secretion in the obese patients.     

A hemodynamic comparison of young and older endurance athletes during exercise

This study assessed the hemodynamic responses to exercise of master athletes (56 +/- 5 yr of age) who placed in the top 10% of their age groups in local 10-km competitive events, competitive young runners (26 +/- 3 yr), young runners matched in training and performance to the master athletes (25 +/- 3 yr), and healthy older sedentary subjects (58 +/- 5 yr). The maximal O2 consumption (VO2max) of the master athletes was 9 and 19% lower than that of the matched young and competitive young runners, respectively. When compared at the same relative submaximal work rates, these three groups had similar stroke volumes and arteriovenous O2 (aVO2) differences, though the master athletes had lower VO2, cardiac output, and heart rate, and higher vascular resistance. The older sedentary group had a lower stroke volume, aVO2 difference, and higher vascular resistance than the master athletes. Maximal stroke volume and estimated aVO2 difference were the same in the three groups of athletes; the lower maximal heart rate of the master athletes appears to account for their lower VO2max. The older sedentary subjects' VO2max was 47% lower than that of the master athletes; this difference was almost equally the result of a lower stroke volume and a lower a-VO2 difference. Thus these older athletes did not exhibit the decline in maximum stroke volume and aVO2 difference that occurs with aging in sedentary individuals; they also appear to have retained a greater peripheral vasodilatory response than their sedentary peers.     

Resistance and aerobic exercise: the influence of mode on the relationship between IL-6 and glucose tolerance in young men who are obese

Regular exercise lowers indicators of disease risk including some inflammatory cytokines; however, the relationship between different modes of acute exercise, cytokine levels, and subsequent glucose tolerance is unclear. The purpose was to determine the effects of resistance (RES) and aerobic (AER) exercises on interleukin-6 (IL-6) and its association with glucose tolerance 24 hours after exercise. After testing for 1 repetition maximum (1RM) and VO2peak, 10 obese (body mass index > 30 kg · m(-2)), untrained men aged 18-26 years completed 3 protocols: 60 minutes of RES, AER, and a resting (CON) condition. The RES was 2 sets of 8 repetitions and a third set to fatigue at 80% 1RM of 8 lifts using all major muscle groups. The AER was 60 minutes of cycling at 70% of VO2peak. On day 1, subjects completed the 60-minute exercise or resting protocol, and on day 2, they completed an oral glucose tolerance test (OGTT). Blood was collected before and after exercise, at 2 and 7 hour postexercise, and before and every 30 minutes during the OGTT and was analyzed for IL-6, glucose and insulin. Postexercise IL-6 was greater in RES (8.01 ± 2.08 pg · mL(-1)) vs. in AER (4.26 ± 0.27 pg · mL(-1)), and both were greater than in CON (1.61 ± 0.18 pg · mL(-1)). During the OGTT, there were no differences in glucose or insulin between conditions for single time points or as area under the curve. The RES caused greater IL-6 levels immediately after exercise that may be related to the greater active muscle mass compared to AER. Neither exercise produced enhanced glucose removal compared to control; thus, despite the greater elevation in IL-6 in RES, for these exercise conditions and this population, this cytokine did not influence glucose tolerance.     

Effect of a two-month detraining on glucose tolerance and insulin sensitivity in athletes--link to adrenal steroid hormones

Reduction in physical activity has been demonstrated to associate with the increased risk in insulin resistance and type 2 diabetes. To determine whether alteration in insulinemia, due to abstention from regular exercise training, is associated with changes in serum dehydroepiandrosterone sulfate (DHEA-S) and cortisol, 18 highly trained badminton players (21.2 +/- 0.3 years) were enrolled into a 2-month detraining study. Fasting serum insulin, glucose, DHEA-S, and cortisol were determined at trained state and at day 60 of detraining. Glucose tolerance and insulin sensitivity were assessed by an oral glucose tolerance test (OGTT). The 2-month detraining increased fasting glucose and insulin concentrations and body weight slightly, but did not significantly affect glucose tolerance and insulin response curve, in which 10 subjects had increased and 8 subjects had slightly decreased in the area under curve for insulin (IAUC). In the subjects with increased IAUC, serum cortisol was also elevated (from 0.44 +/- 0.07 to 0.83 +/- 0.26 U/l, P < 0.05) in parallel, and serum creatine kinase (CK) was unaltered during detraining. Whereas in the subjects with decreased IAUC, serum cortisol (from 0.51 +/- 0.19 to 0.54 +/- 0.14 U/l, no significance) was not changed and serum creatine kinase (from 461 +/- 179 to 151 +/- 21 U/l) was decreased during detraining. Two groups of detrained subjects exhibited a similar reduction in serum DHEA-S levels and slight elevation in body weight. The novel finding of the study is that the changes in serum cortisol, but not DHEA-S, were associated with the change in insulin sensitivity during early phase of lifestyle change from physically active to sedentary, and this response appears to be varied individually among athletes.     

Assessing Impaired Glucose Tolerance and Insulin Resistance in Polycystic Ovarian Syndrome with A Muffin Test: An Alternative to the Glucose Tolerance Test

ObjectiveTo determine the sensitivity of a high-glucose load in a meal as an alternative to the standard oral glucose tolerance test (OGTT) in detecting impaired glucose tolerance and insulin resistance in women with polycystic ovarian syndrome (PCOS) and the relationship of body composition to insulin resistance in the PCOS cohort.MethodsIn this prospective, single-center study, women with PCOS who were being followed up as outpatients were recruited. The study was performed between November 2007 and March 2008. All participants underwent OGTT before study enrollment. Participants were given a meal including carbohydrates, fat, and protein. Glucose and insulin levels were measured every 30 minutes for 2 hours after completing the meal. Body composition was measured by dual-energy x-ray absorptiometry.ResultsThirteen of the 15 participants completed the meal tolerance test and the body composition study. Four of 13 participants (31%) had abnormal glucose tolerance with the meal test compared with 2 of 8 participants (25%) who completed the OGTT. Those who had insulin resistance on OGTT were detected with the meal test. The 2-hour insulin levels following the meal were 38% higher than with the OGTT. Of 10 participants with insulin resistance, 9 had a total body fat mass greater than the 90th percentile, whereas 1 of 3 participants (33%) with normal body composition was insulin resistant.ConclusionAdministration of oral glucose load via a meal is an effective alternative to the OGTT in diagnosing impaired glucose tolerance and insulin resistance and may be more sensitive, without the adverse effects of the oral glucose load in the OGTT. PCOS is an independent risk factor for impaired glucose tolerance and insulin resistance, regardless of body composition. (Endocr Pract. 2010;16:810-817)     

Exercise-induced pyruvate dehydrogenase activation is not affected by 7 days of bed rest

To test the hypothesis that physical inactivity impairs the exercise-induced modulation of pyruvate dehydrogenase (PDH), six healthy normally physically active male subjects completed 7 days of bed rest. Before and immediately after the bed rest, the subjects completed an oral glucose tolerance test (OGTT) and a one-legged knee extensor exercise bout [45 min at 60% maximal load (W(max))] with muscle biopsies obtained from vastus lateralis before, immediately after exercise, and at 3 h of recovery. Blood samples were taken from the femoral vein and artery before and after 40 min of exercise. Glucose intake elicited a larger (P ≤ 0.05) insulin response after bed rest than before, indicating glucose intolerance. There were no differences in lactate release/uptake across the exercising muscle before and after bed rest, but glucose uptake after 40 min of exercise was larger (P ≤ 0.05) before bed rest than after. Muscle glycogen content tended to be higher (0.05< P ≤ 0.10) after bed rest than before, but muscle glycogen breakdown in response to exercise was similar before and after bed rest. PDH-E1α protein content did not change in response to bed rest or in response to the exercise intervention. Exercise increased (P ≤ 0.05) the activity of PDH in the active form (PDHa) and induced (P ≤ 0.05) dephosphorylation of PDH-E1α on Ser2?3, Ser2?? and Ser3??, with no difference before and after bed rest. In conclusion, although 7 days of bed rest induced whole body glucose intolerance, exercise-induced PDH regulation in skeletal muscle was not changed. This suggests that exercise-induced PDH regulation in skeletal muscle is maintained in glucose-intolerant (e.g., insulin resistant) individuals.     

Effect of a single bout of resistance exercise on postprandial glucose and insulin response the next day in healthy, strength-trained men

Postprandial blood glucose and insulin levels are both risk factors for developing obesity, type-2 diabetes, and coronary heart diseases. To date, research has shown that a single bout of moderate- to high-intensity aerobic exercise performed 相似文献   

Seven days of aerobic exercise training improves conduit artery blood flow following glucose ingestion in patients with type 2 diabetes

The vasodilatory effects of insulin account for up to 40% of insulin-mediated glucose disposal; however, insulin-stimulated vasodilation is impaired in individuals with type 2 diabetes, limiting perfusion and delivery of glucose and insulin to target tissues. To determine whether exercise training improves conduit artery blood flow following glucose ingestion, a stimulus for increasing circulating insulin, we assessed femoral blood flow (FBF; Doppler ultrasound) during an oral glucose tolerance test (OGTT; 75 g glucose) in 11 overweight or obese (body mass index, 34 ± 1 kg/m2), sedentary (peak oxygen consumption, 23 ± 1 ml·kg?1·min?1) individuals (53 ± 2 yr) with non-insulin-dependent type 2 diabetes (HbA1c, 6.63 ± 0.18%) before and after 7 days of supervised treadmill and cycling exercise (60 min/day, 60-75% heart rate reserve). Fasting glucose, insulin, and FBF were not significantly different after 7 days of exercise, nor were glucose or insulin responses to the OGTT. However, estimates of whole body insulin sensitivity (Matsuda insulin sensitivity index) increased (P < 0.05). Before exercise training, FBF did not change significantly during the OGTT (1 ± 7, -7 ± 5, 0 ± 6, and 0 ± 5% of fasting FBF at 75, 90, 105, and 120 min, respectively). In contrast, after exercise training, FBF increased by 33 ± 9, 39 ± 14, 34 ± 7, and 48 ± 18% above fasting levels at 75, 90, 105, and 120 min, respectively (P < 0.05 vs. corresponding preexercise time points). Additionally, postprandial glucose responses to a standardized breakfast meal consumed under "free-living" conditions decreased during the final 3 days of exercise (P < 0.05). In conclusion, 7 days of aerobic exercise training improves conduit artery blood flow during an OGTT in individuals with type 2 diabetes.     

Effect of prior exercise on glucose metabolism in trained men

Several studies have demonstrated that oral glucose tolerance is impaired in the immediate postexercise period. A double-tracer technique was used to examine glucose kinetics during a 2-h oral glucose (75 g) tolerance test (OGTT) 30 min after exercise (Ex, 55 min at 71 +/- 2% of peak O(2) uptake) and 24 h after exercise (Rest) in endurance-trained men. The area under the plasma glucose curve was 71% greater in Ex than in Rest (P = 0.01). The higher glucose response occurred even though whole body rate of glucose disappearance was 24% higher after exercise (P = 0.04, main effect). Whole body rate of glucose appearance was 25% higher after exercise (P = 0.03, main effect). There were no differences in total (2 h) endogenous glucose appearance (R(a)E) or the magnitude of suppression of R(a)E, although R(a)E was higher from 15 to 30 min during the OGTT in Ex. However, the cumulative appearance of oral glucose was 30% higher in Ex (P = 0.03, main effect). There were no differences in glucose clearance rate or plasma insulin responses between the two conditions. These results suggest that adaptations in splanchnic tissues by prior exercise facilitate greater glucose output from the splanchnic region after glucose ingestion, resulting in a greater glycemic response and, consequently, a greater rate of whole body glucose uptake.     

Impaired beta-cell compensation to dexamethasone-induced hyperglycemia in women with polycystic ovary syndrome

Deterioration in glucose tolerance occurs rapidly in women with polycystic ovary syndrone (PCOS), suggesting that pancreatic beta-cell dysfunction may supervene early. To determine whether the compensatory insulin secretory response to an increase in insulin resistance induced by the glucocorticoid dexamethasone differs in women with PCOS and control subjects, we studied 10 PCOS and 6 control subjects with normal glucose tolerance. An oral glucose tolerance test (OGTT) and a graded glucose infusion protocol were performed at baseline and after subjects took 2.0 mg of dexamethasone orally. Basal (Phi(b)), static (Phi(s)), dynamic (Phi(d)), and global (Phi) indexes of beta-cell sensitivity to glucose were derived. Insulin sensitivity (S(i)) was calculated using the minimal model; a disposition index (DI) was calculated as the product of S(i) and Phi. PCOS and control subjects had nearly identical fasting and 2-h glucose levels at baseline. Phi(b) was higher, although not significantly so, in the PCOS subjects. The Phi(d), Phi(s), and Phi indexes were 28, 19, and 20% higher, respectively, in PCOS subjects. The DI was significantly lower in PCOS (30.01 +/- 5.33 vs. 59.24 +/- 7.59) at baseline. After dexamethasone, control subjects averaged a 9% increase (to 131 +/- 12 mg/dl) in 2-h glucose levels; women with PCOS had a significantly greater 26% increase to 155 +/- 6 mg/dl. The C-peptide-to-glucose ratios on OGTT increased by 44% in control subjects and by only 15% in PCOS subjects. The accelerated deterioration in glucose tolerance in PCOS may result, in part, from a relative attenuation in the response of the beta-cell to the demand placed on it by factors exacerbating insulin resistance.     

Assessment of insulin resistance in normoglycemic young adults

Detection of Insulin resistance (IR) in normoglycemic young subjects before the onset of Impaired Glucose Tolerance (IGT) is of importance as it affords implementation of preventive measures in such high risk subject. Very few studies have specifically evaluated for the presence of IR in younger age group with normal glucose tolerance. The gold standard for investigating and quantifying insulin resistance is the “hyperinsulinemic euglycemic clamp,” the complicated nature of the “clamp” technique, alternatives have been sought to simplify the measurement of insulin resistance. The oral glucose tolerance test (OGTT) is one of the most commonly used methods to evaluate whole body glucose tolerance in vivo. IR and IS values of HOMA-IR, ISI_0–120, QUICKIE mathematical models derived from OGTT have been shown to produce equivalent results as in Euglycemic clamp technique we hypothesized that normoglycemic young adult who are siblings of type II diabetics (SD) probably have higher IR values than the siblings of non diabetics as they are genetically predisposed.     

New metabolic interdependencies revealed by plasma metabolite profiling after two dietary challenges

Oral glucose tolerance tests (OGTT) are valuable tools for diagnosis of impaired glucose tolerance and insulin resistance. Protein intake modulates insulin secretion and sensitivity and thereby can alter the metabolic response. To assess these effects in the plasma metabolome, 15 healthy human volunteers underwent in random order an OGTT with and without 30?g of a protein-hydrolysate (OGTT?+?PL) followed by metabolite profiling via LC?CMS/MS. Compared to the OGTT alone, plasma glucose response was reduced and insulin clearance retarded after OGTT?+?PL while suppression of catabolic markers such as free fatty acids, glycerol, lactate or acylcarnitines showed no difference between the two challenges. Clusters of plasma amino acids characterized by subgroups with similar physico-chemical characteristics revealed long-lasting declines after the OGTT and coherent increases after the OGTT?+?PL despite the fact that the protein-hydrolysate provided different amounts of individual amino acids. The amino acid clusters identified appear to derive from common transport processes involved in intestinal absorption and the insulin-dependent extraction by target tissues and suggest that these processes may be of high diagnostic value to assess insulin sensitivity.