[Importance of the post-prandial glycemia in the management of type 2 diabetes]. / Importance de la glycémie postprandiale dans la prise en charge du diabète de type 2.

Cardiovascular disease is the main cause of mortality in diabetic patients. The risk of cardiovascular disease occurs at a lower glycemic level compared to microvascular complications. Post-prandial hyperglycemia seems to play a major role in the development of atherosclerotic lesions. In this article we review the evidence regarding the prognostic value of post-challenge hyperglycaemia relative to the risk of cardiovascular disease, explore the physio-pathologic mechanisms responsible for the negative effects of post-prandial hyperglycaemia and detail the benefits of treatment aimed at controlling post-prandial glycaemia.

[Diabetes mellitus and driving]. / Diabète sucré et conduite automobile.

Most studies, which are retrospective, show contradictory results regarding the incidence of road traffic accident among diabetic patients. The most frequent cause of accident is hypoglycemia. One should also consider impaired vision (retinopathy, maculopathy), neuropathy (feet insensitivity) and sleep apnoea in overweight patients. Hypoglycemia not only leads to impaired judgement during driving, but also to a reduction in performances, frequent hypoglycemias impair symptom recognition and increase the risk of loss of consciousness. Patients should benefit from teaching about hypoglycemia, i.e. how to recognize and correct it in order to avoid accidents. Generally they should not drive if their glycemia is under 5 mmol/l without correcting it with an adequate amount of carbohydrates.

Parenteral nutrition practices in hospital pharmacies in Switzerland, France, and Belgium.

OBJECTIVE: Important changes in administering total parenteral nutrition (PN) admixtures have occurred over the past decade. This study describes hospital pharmacists' practices in France (F), Switzerland (CH), and Belgium (B). METHODS: From the responses received using a standardized questionnaire, (n = 378) we determined the origin, types of container used, and choice of PN formula (standard versus tailor-made) and the type of quality control and the existence of nutrition support teams. RESULTS: The mean response rates were 55.6% (CH), 30.5% (F), and 24.5% (B). Standard formulas were used mainly for adult patients (CH, 86%; F, 79%; B, 86%), whereas approximately 50% of tailor-made PN bags were used for children. Single-compartment or multicompartment bags or glass bottles contained standard formulas. Most standard formulas were provided by industry, apart from (B), where 50% of PN solutions were compounded by hospital pharmacies. Single-compartment bags contained generally tailor-made formulas produced exclusively by hospital pharmacies in (CH) and (B), whereas 33% were provided by industry in (F). Quality controls were mostly visual and occurred in 75% to 95% of hospitals. Nutrition support teams were present in 32% to 45% of hospitals. CONCLUSION: The choice, origin, and type of container used for PN formulas were highly variable among countries. However, the use of standard formulas in bags was predominant in (CH) and (B). The function of nutrition support teams was similar in (F), (CH), and (B).

Five-year follow-up after pediatric living related small bowel transplantation between two monozygotic twins.

Two 13-year-old monozygotic twins were used for living related small bowel transplantation (SBTx). The recipient presented with short gut syndrome secondary to complicated abdominal surgery. The indication for SBTx was based on a failure to thrive and a poor tolerance of TPN. The donor was an identical twin, as demonstrated by skin graft acceptance, which allowed performance of SBTx without immunosuppression. Growth charts were used to follow intestinal absorption functions and body composition. The donor was used as a control for the recipient. The recipient, who was transplanted with 160 cm of donor ileum, was discharged on postoperative day 62 on a regular diet. Before SBTx the recipient was 10 kg lighter in body weight than the donor, a gap that was progressively reduced over the follow-up period. A height deficit of 3 cm reversed within 1 year after SBTx. A 10-kg deficit in fat-free body mass was completely extinguished within 18 months. By 18 months posttransplant, recipient serum albumin and prealbumin were normal and comparable to donor values. d-Xylose absorption in the recipient remained lower than that in the donor. Within 6 months fecal fat excretion normalized in the recipient. d-Xylose absorption and fecal fat excretion were always within a normal range in the donor.

Food intake in 1707 hospitalised patients: a prospective comprehensive hospital survey.

BACKGROUND & AIMS: This study aimed to assess the ability of the hospital meal service to meet patients' nutritional needs. METHODS: All hospitalised patients who received 3 meals/day without artificial nutritional support were included. The nutritional values of food served, consumed and wasted during a 24 h period were compared to patients' needs estimated as energy: 110% Harris-Benedict formula; protein: 1.2 or 1.0 g/kg bodyweight/day for patients < or = or > 65 years old, respectively. A structured interview recorded patients' evaluation of the meal quality, their reasons for non-consumption of food and the relationship between food intake and disease. RESULTS: Out of 1707 patients included, 1416 were fully assessable (59% women; 68+/-21 years; body mass index: 24.3+/-5.1 kg/m(2)). Daily meals provided 2007+/-479 kcal and 78+/-21 g of protein and exceeded patients' needs by 41% and 15%, respectively. However, 975 patients did not eat enough. Plate waste was 471+/-372 kcal and 21+/-17 g of protein/day/patient. Moreover, the food intake of 572 (59%) of these underfed patients was not predominantly affected by disease. Logistic regression analyses identified as other risk factors: elevated BMI, male gender, modified diet prescription, length of stay <8 or > or = 90 days and inadequate supper. CONCLUSION: Despite sufficient food provision, most of the hospitalised patients did not cover their estimated needs. Since insufficient food intake was often attributed to causes other than disease, there should be potential to improve the hospital meal service.

Four year nutritional follow up after living related small bowel transplantation between monozygotic twins.

While small bowel transplantation (SBTX) may allow parenteral nutrition independence in the case of short bowel syndrome, its effects on body composition and growth are unclear. For the first time, a paediatric living related SBTX was performed between monozygotic twins. This case report describes their four year nutritional follow up. The 13 year old recipient and his healthy brother underwent measurements of body composition by 50 kHz bioimpedance analysis and bone mineral density of the femoral neck and total femur by dual energy x ray absorptiometry. Xylose tests and measurements of faecal fat evaluated gut absorption. All tests were performed before and after SBTX. Body weight increased from 34.7 to 51.9 kg in the recipient and from 45.0 to 53.2 kg in the donor within four years. The recipient caught up with the height and fat free mass of his brother within two years. Fat mass, and total femur and femoral neck densities are still lower in the recipient than in the donor four years after SBTX (-1.2 kg, -0.087 g/cm(2), -0.035 g/cm(2)). The xylose test of the recipient was still abnormally low after four years (1.37 mmol/l) and faecal fat was high until two years after SBTX (March 2001: 12 g/24 h). The donor always showed normal xylose tests and faecal fat, except for one episode of high faecal fatty acids about 10 months after SBTX. SBTX improved the nutritional state and growth of the graft recipient although body composition, femoral bone mineral densities, and intestinal absorption had not completely normalised after four years.

Protective effects of recombinant growth hormone on intestinal mucosa in rats receiving abdominal radiotherapy.

BACKGROUND AND AIMS: Radiation injury to the gut induces nutrient losses that compromise the body ability to adequately fight infection, heal wounds and recover from illness. Recombinant growth hormone (rhGH), is known to enhance anabolism, therefore, we tested the hypothesis that rhGH preserves whole body growth and trophism of the jejunum and ileum of irradiated rats. METHODS: After acclimatization period, the rats were divided in three groups: (1). control rats (C), (2). rats irradiated with a single dose of 10 Gy (group A); (3). rats irradiated with a single dose of 5 Gy (Group B); after irradiation, rats were given subcutaneously (sc) saline or 0.25 or 0.50 mg rhGH/kg BW/d for the following 6 days. Body weight changes were recorded during this time. On day 6 post-radiation, rats were killed and small intestine mucosa dry and wet weights were measured, as well as mucosa protein content. RESULTS: Group A rats lost body weight during the 6-day post-radiation period, regardless of rhGH treatment and dosage. rhGH was effective in preventing weight loss and normalizing growth in group B rats (saline 23.1+/-11.1, vs. controls P<0.05; rhGH: 35.0+/-10.0 g BW/d, vs. controls P = ns). Trophic effect of rhGH was observed on mucosa weight and mucosa protein content in rats irradiated with 5 Gy, but not in those receiving 10 Gy. CONCLUSION: rhGH seems to normalize growth and mucosa protein content in irradiated rats. However, rhGH beneficial effects were observed only in rats receiving the lower dose of radiation.

Management of catabolism in metabolically stressed patients: a literature survey about growth hormone application.

In the effort to improve the long-term outcome in critically ill patients, the utilization of anabolic agents, such as human recombinant growth hormone, has been proposed in order to reduce catabolism and improve nutritional status. A recent multicentre study regarding the use of human recombinant growth hormone in intensive care unit patients showed an unexpected increase in the mortality rate in human recombinant growth hormone-treated patients. This finding is in contrast with previous literature data reporting either no differences or an even lower mortality rate with the administration of human recombinant growth hormone. This review evaluates the possible reasons for this dramatic difference in outcomes between the multicentre study and the existing literature. Articles dealing with human recombinant growth hormone administration either in intensive care unit patients (n=26) or in postoperative patients (n=16) have been reviewed. Our analysis suggests that the low caloric intake given to patients enrolled in the multicentre study might have been inadequate to compensate for the hypermetabolism of these patients, and could not support the prolonged and delayed administration of high doses of human recombinant growth hormone. Whether the beneficial metabolic effects of human recombinant growth hormone translate into better clinical outcomes deserves further investigation. In addition, the careful selection of patients to be treated, and close monitoring of both the adequacy of caloric support and modality of human recombinant growth hormone administration would favour the safety of human recombinant growth hormone utilization in critical care settings.

Rates of urea production and hydrolysis and leucine oxidation change linearly over widely varying protein intakes in healthy adults.

The quantitative relationships between nitrogen (N) intake, urea production, excretion and amino acid oxidation are currently a matter of debate. Some investigators have proposed that urea production is essentially constant over a wide range of N intakes and that urea hydrolysis is regulated according to the N needs of the organism. We have assessed this proposal by compiling results from four separate experiments in healthy young adults (n = 34) carried out in our laboratories and all at the end of the respective diet periods using an identical 24-h continuous intravenous infusion of [(15)N, (15)N]urea and L-[1-(13)C]leucine. The N intakes were: expt. 1; protein-free diet for 5 d; expt. 2; N at 44 mg N. kg(-1). d(-1) from a balanced L-amino acid mixture for 13 d; expt. 3; N at 161 mg. kg(-1). d(-1) from egg protein for 6 d; expt. 4 -one group received 157 mg. kg(-1). d(-1) and the other 392 mg. kg(-1). d(-1) from milk-protein-based diets for 6 d. Urea production and excretion were linearly correlated with N intake (r = 0.98 and 0.94, respectively; P < 0.01). Urea hydrolysis increased linearly with N intake (r = 0.7; P < 0.05), with considerable variation in the rate among individuals, especially at the N intake of approximately 160 mg N. kg(-1)d(-1). These findings are consistent with the generally accepted view that a control of body N balance is via a regulation of urea production. They do not support the concept that urea hydrolysis is the more important site in the control of body N loss.

Fat metabolism during high-intensity exercise in endurance-trained and untrained men.

To determine whether trained individuals rely more on fat than untrained persons during high-intensity exercise, six endurance-trained men and six untrained men were studied during 30 minutes of exercise at 75% to 80% maximal oxygen consumption (VO2max). The rates of appearance (Ra) and disappearance (Rd) of glycerol and free fatty acids (FFAs) were determined using [1,1,2,3,3-2H]glycerol and [1-13C]palmitate, respectively, whereas the overall rate of fatty acid oxidation was determined using indirect calorimetry. During exercise, the whole-body rate of lipolysis (ie, glycerol Ra) was higher in the trained group (7.1 +/- 1.2 v 4.5 +/- 0.7 micromol x min(-1) x kg(-1), P < .05), as was the Ra (approximately Rd) of FFA (9.0 +/- 0.9 v 5.0 +/- 1.0 micromol x min(-1) x kg(-1), P < .001). FFA utilization was higher in trained subjects even when expressed as a percentage of total energy expenditure (10% +/- 1% v 7% +/- 1%, P < .05). However, this difference in plasma FFA flux could not account for all of the difference in fatty acid oxidation between trained and untrained subjects (20.8 +/- 3.3 v 7.9 +/- 1.6 micromol x min(-1) x kg(-1), or 23% +/- 3% v 13% +/- 2% of total energy expenditure, both P < .05). Thus, the oxidation of fatty acids derived from some other source also must have been greater in the trained men. We conclude that trained athletes use more fat than untrained individuals even during intense exercise performed at the same percentage of VO2max. The additional fatty acids appear to be derived from both adipose tissue and, presumably, intramuscular triglyceride stores.

Cysteine kinetics and oxidation at different intakes of methionine and cystine in young adults.

BACKGROUND: We previously studied methionine kinetics and oxidation with the tracer L-[1-(13)C, methyl-(2)H(3)]methionine. OBJECTIVES: We sought to explore methionine-cysteine interrelations in adults by using L-[1-(13)C]cysteine under different dietary conditions. DESIGN: In experiment 1, 12 adults consumed a protein-free diet for 6 d. On day 7, methionine (n = 6) or cysteine (n = 6) oxidation rates were measured during an 8-h continuous infusion of L-[1-(13)C, methyl-(2)H(3)]methionine or L-[1-(13)C]cysteine, respectively. In experiment 2, 6 young men consumed 3 diets for 6 d each before a tracer study on day 7 with L-[1-(13)C]cysteine. The amounts (in mg*kg(-)(1)*d(-)(1)) of methionine and cysteine, respectively, were: high-methionine (HM) diet, 13 and 0; low-methionine (LM) diet, 6.5 and 0; and methionine-plus-cystine (MC) diet, 6.5 and 5.6. Cysteine flux and oxidation rates were determined and sulfur amino acid (SAA, methionine plus cysteine) balances were estimated. RESULTS: In experiment 1, rates of methionine and cysteine oxidation were similar to losses predicted from obligatory nitrogen losses. In experiment 2, SAA balance was less negative when subjects consumed the HM diet than the LM and MC diets (interaction, P = 0.034), largely because of a difference in fed-state balance (HM compared with LM, P < 0.01; HM compared with MC, P < 0.05). There was no evidence of a sparing effect of dietary cystine on the methionine requirement. CONCLUSION: These studies support use of [1-(13)C]cysteine for studying whole-body SAA oxidation and conclusions that maintenance of SAA balance is best achieved by supplying methionine at approximately the FAO/WHO/UNU recommendations for total SAA intake (13 mg*kg(-)(1)*d(-)(1)).

Leucine kinetics in reference to the effect of the feeding mode as three discrete meals.

In a recent study, we observed that the 24-hour leucine oxidation measured when three equal meals providing a generous intake of leucine (approximately 90 mg x kg(-1) x d(-1)) are eaten during the day is 16% lower (P < .01) than that for the same diet given as 10 hourly, equal meals. We hypothesized that the pattern of meal intake at a lower level of dietary leucine would affect the 24-hour rate of leucine oxidation and possibly improve the retention of dietary leucine. A total of 11 healthy adults participated in this investigation. The daily leucine intake was 182 micromol x kg(-1) x d(-1) (38 mg x kg(-1) x d(-1)) given with an L-amino acid diet. All subjects received three discrete meals daily for 6 days prior to a 24-hour intravenous (IV) tracer infusion of L-[1-13C]-leucine on day 7 (study 1). Four of these subjects participated in two additional studies of similar design. Study 2 involved giving [1-13C]-leucine as a constant IV infusion together with tracer added to the amino acid mixture at each meal time. In study 3, subjects received the three meals with added [1-13C]-leucine tracer while [2H3]-leucine was given as a constant IV infusion. Total leucine oxidation in studies 1 and 2 was 238+/-66 and 231+/-85 micromol x kg(-1) x d(-1), respectively. Leucine balance was positive, amounting to 18% of the total (diet + tracer) intake. The estimated mean nitrogen balance was +8 mg x kg(-1) x d(-1). Leucine oxidation was higher (P < .01) for breakfast than for the lunch meal. This difference was associated with lower insulin and higher plasma leucine concentrations at breakfast versus lunch periods. The results from study 3 suggest that the higher rate of leucine oxidation observed at breakfast as compared with lunch is not due to a difference in the immediate splanchnic fate of absorbed leucine from each meal. In comparison to our previous small frequent-meal studies, the pattern of meal feeding influences overall leucine utilization at both generous and limiting leucine intakes. Hence, it is possible that the pattern of meal feeding may affect estimations of amino acid requirements using the tracer-balance approach. Longer-term dietary studies will be needed to establish whether and the extent to which this is so.

A tracer investigation of obligatory oxidative amino acid losses in healthy, young adults.

BACKGROUND: Estimation of the minimum requirement for indispensable amino acids (IAAs) has been attempted by assuming that obligatory oxidative losses (OOLs) of IAAs can be approximated from nitrogen losses and that the efficiency of utilization of IAAs at requirement intakes is approximately 70%. OBJECTIVE: We wished to determine the rates of OOLs in healthy adults, using L-[1-(13)C]leucine and L-[1-(13)C, methyl-(2)H(3)]methio-nine as tracers, after adjustment to a protein-free diet and how these rates compare with those when either sulfur amino acids (SAAs: methionine and cyst(e)ine) or leucine were removed from an otherwise adequate diet. DESIGN: Eleven subjects were randomly assigned to a 5-d protein-free diet or a 5-d diet providing adequate nitrogen and amino acids except for the SAAs or leucine. A 24-h constant intravenous infusion of [(15)N, (15)N]urea and L-[1-(13)C]leucine (Leu group; n = 5) or L-[1-(13)C, methyl-(2)H(3)]methionine (Met group; n = 6 ) began at 1800 on day 5 and rates of amino acid oxidation were determined. RESULTS: Mean (+/-SD) oxidation rates (mg kg(-)(1) d(-)(1)) of methionine and leucine were 6.4 +/- 1.4 and 24.7 +/- 3.6, respectively, with the protein-free diet; rates were significantly lower (3.9 +/- 2.2 and 7. 2 +/- 3.4, respectively) after the SAA- and leucine-free diets. Urea production was significantly lower (P < 0.01) with the protein-free than with the SAA- or leucine-free diet. CONCLUSIONS: Isotopically determined OOLs for methionine and leucine are consistent with losses predicted from nitrogen excretion, and consistent with our previous measurements of cysteine oxidation as an index of total SAA losses. The data further support our earlier conclusions regarding methionine sparing by cysteine and tentative recommended SAA requirements in adults.

Effect of cystine intake on methionine kinetics and oxidation determined with oral tracers of methionine and cysteine in healthy adults.

There is evidence based on nitrogen balance that dietary cystine spares, from approximately 16% to 89%, the total methionine requirement. In a previous study we did not detect, by tracer techniques, a sparing effect of cystine when the diet provided methionine at a limiting intake (requirement level: 13 mg.kg-1.d-1). One reason could be that we used an intravenous infusion of the tracer, which may not, therefore, have labeled the carbon dioxide derived from the splanchnic oxidation of dietary methionine. The aim of this study was to compare methionine metabolism and oxidation in eight healthy adults given for 6 d each of three different diets: 13 mg (87.0 mumol) methionine.kg-1.d-1 and no cystine (diet A); 5 mg (33.5 mumol) methionine.kg-1.d-1 and no cystine (diet B); and 5 mg (33.5 mumol) methionine.kg-1.d-1 and 6.5 mg (52.4 mumol) cystine.kg-1.d-1 (diet C). On day 7, tracers ([1-13C, methyl-2H3]methionine and [2H2]cysteine) were administered orally at 30-min intervals for 8 h. Blood and breath samples were obtained for analysis during 3-h fasting and consecutive 5-h feeding periods. During fasting, methionine oxidation and methionine methyl (Qm) and carboxyl (Qc) fluxes and plasma concentrations were not affected by the amount of sulfur amino acids in the three diets. In the fed state methionine oxidation was significantly lower during diets B (3.0 +/- 0.5 mumol.kg-1.h-1) and C (2.8 +/- 0.6 mumol.kg-1.h-1) than during diet A (4.1 +/- 0.9 mumol.kg-1.h-1); there were no significant differences between diets B and C. Qm and Qc decreased with decreased methionine intake but no effect was observed by adding cystine. Cysteine flux (Qcys) was not affected by diet composition but it was lower during feeding than during fasting. In conclusion, replacing approximately 60% of the total requirement for methionine with cystine over a short diet period did not result in a detectable sparing of methionine oxidation.

Regulation of glucose production during exercise at 80% of VO2peak in untrained humans.

To determine whether alterations in insulin and/or glucagon secretion play an important role in stimulating glucose production (Ra) during intense but submaximal exercise, we studied six untrained subjects during 30 min of cycling at 80% of peak oxygen uptake on two occasions: once under control conditions and once when alterations in insulin and glucagon secretion were prevented with the use of the pancreatic islet clamp technique. In the latter experiments, glucose was infused during exercise to match glycemia with control levels. Glucose kinetics were measured in both trials using a primed, continuous infusion of [6,6-2H]glucose. In the control trial, glucose Ra rose from 11.9 +/- 0.8 mumol.min-1.kg-1 at rest to 42.5 +/- 4.3 mumol.min-1.kg-1 by the end of exercise. A similar increment was observed in the islet clamp experiments, with endogenous Ra peaking at 37.2 +/- 7.9 mumol.min-1.kg-1. This was true even through glucagon concentration did not change from basal and insulin concentration actually rose (the latter apparently due to a decrease in insulin clearance during intense exercise). Thus neither decrements in insulin or increments in glucagon are apparently required to stimulate glucose Ra under the present conditions. Because epinephrine levels rose only slightly, it appears that either neurally released norepinephrine or some other, as yet unidentified, factor is responsible for stimulating glucose Ra during intense but submaximal exercise.

Effect of theophylline on substrate metabolism during exercise.

We tested the hypothesis that adenosine is involved in regulating substrate metabolism during exercise. Seven trained cyclists were studied during 30 minutes of exercise at approximately 75% maximal oxygen uptake (VO2max). Lipid metabolism was evaluated by infusing [2H5]glycerol and [1-13C]palmitate, and glucose kinetics were evaluated by infusing [6,6-2H]glucose. Fat and carbohydrate oxidation were also measured by indirect calorimetry. The same subjects performed two identical exercise tests, but in one trial theophylline, a potent adenosine receptor antagonist, was infused for 1 hour before and throughout exercise. Theophylline did not increase whole-body lipolysis (glycerol rate of appearance [Ra]) or free fatty acid (FFA) release during exercise, but fat oxidation was lower than control values (9.5 +/- 3.0 v 18.0 +/- 4.2 micromol x min(-1) x kg(-1), P < .01). Glucose Ra was not affected by theophylline infusion, but glucose uptake was lower (31.6 +/- 4.1 v 40.4 +/- 5.0 micromol x min(-1) x kg(-1), P < .05) and glucose concentration was higher (6.4 +/- 0.6 v 5.8 +/- 0.4 mmol/L, P < .05) than in the control trial. Total carbohydrate oxidation (302.3 +/- 26.2 v 265.5 +/- 11.7 micromol x min(-1) x kg(-1), P < .06), estimated muscle glycogenolysis (270.7 +/- 23.1 v 225.1 +/- 9.7 micromol x min(-1) x kg(-1), P < .05), and plasma lactate concentration (7.9 +/- 1.6 v 5.9 +/- 1.1 mmol/L, P < .001) were also higher during the theophylline trial. These data suggest that adenosine may play a role in stimulating glucose uptake and restraining glycogenolysis but not in limiting lipolysis during exercise.

Twenty-four-hour energy and nutrient balance in weight stable postobese patients after biliopancreatic diversion.

To better understand the long-term weight stability of postobese patients who underwent biliopancreatic diversion (BPD), we studied 24-h energy and nutrient balance in eight women at least 3 yr after surgery (PO) and compared the results to those obtained in eight normal never-obese control women (C), matched by age and weight. Body composition was measured by dual-energy x-ray absorptiometry (DXA). All the patients were on an ad libitum diet; 24-h energy and nutrient intake were measured on the experimental day. Twenty-four-hour energy expenditure (EE) and 24-h nutrient oxidation rates were measured in a respiratory chamber, and energy and nutrient balances were calculated after correcting for 24-h fecal nutrient loss. No differences in body composition were found between PO and C. PO had a higher gross energy intake than C (10.6 +/- 3.4 vs. 8.0 +/- 2.2 MJ/d; p < 0.05); however, due to the higher energy fecal loss in PO as compared to C (2.4 +/- 1.3 vs. 0.09 +/- 0.01 MJ/day; p < 0.01), 24-h metabolizable energy intake (MEJ) was not different in the two groups. The energy fecal loss in the PO patients was mostly in the form of lipid. EE at 24 h was not different in PO as compared to C. Therefore energy balance, computed as the difference between 24-h MEI and 24-h EE, was similar in the two groups. Respiratory quotient was significantly higher in PO than in C (1.00 +/- 0.08 vs. 0.83 +/- 0.03; p < 0.01). Carbohydrate (-135 +/- 37 g/d in PO vs. 63 +/- 23 g/d in C; p < 0.001), and lipid (48 +/- 14 g/d in PO vs. -23 +/- 6 g/d in C; p < 0.001) balances were different in the two groups. We conclude that chronic lipid malabsorption was the main metabolic abnormality explaining the achievement of energy balance in postobese subjects after biliopancreatic diversion. A chronic reduction of lipid absorption seems to play a key role in the long-term weight stability of this group of postobese subjects.

Lipid and carbohydrate metabolism in IDDM during moderate and intense exercise.

Insulin-dependent diabetes mellitus (IDDM) is characterized by a metabolic and hormonal disarray that may be more evident during exercise. However, the metabolic response to exercise of different intensities has not been evaluated in IDDM. We therefore used stable isotope techniques and indirect calorimetry to quantify substrate kinetics and oxidation during 30 min of exercise at 45 and 75% of maximal oxygen uptake (Vo2max) in seven men with IDDM (D group) infused with insulin at a constant basal rate. Normal control subjects (C group) matched for age, weight, and Vo2max were also studied. During moderate exercise, glucose uptake (Rd) was lower in the D than in the C group (15.3 +/- 1.0 vs. 20.8 +/- 1.6 mumol.min-1.kg-1; P < 0.05). Carbohydrate oxidation also tended to be lower in the D group (71.0 +/- 7.2 vs. 87.5 +/- 10.6 mumol.min-1.kg-1; P = 0.08). The D group relied on fat oxidation to a greater extent than did the C group (16.9 +/- 1.1 vs. 10.4 +/- 1.6 mumol.min-1.kg-1; P < 0.05). The enhanced fat oxidation was not due to increased lipolysis because no differences occurred in glycerol release (Ra) or in plasma free fatty acid Ra or concentration, and the source of the extra lipid appeared to be intramuscular fat stores. These differences in substrate metabolism were not evident during exercise at 75% of Vo2max. The lower glucose uptake and oxidation in the diabetic subjects during moderate, but not intense, exercise suggest that glucose metabolism is regulated differently depending on exercise intensity.(ABSTRACT TRUNCATED AT 250 WORDS)

Glucose kinetics during high-intensity exercise in endurance-trained and untrained humans.

In humans, endurance training reduces the rates of glucose production and utilization during moderate-intensity exercise. It is uncertain, however, whether this is also true during high-intensity exercise. Accordingly, we studied eight endurance-trained cyclists and eight untrained subjects during 30 min of cycling at approximately 80% of maximal oxygen uptake (VO2max). Rates of glucose appearance (Ra) and disappearance (Rd) were determined using a primed, continuous infusion of [6,6-2H]glucose. Average glucose Ra during exercise did not differ in the trained and untrained subjects (34.3 +/- 3.6 vs. 36.0 +/- 1.7 mumol.min-1.kg-1; mean +/- SE; P, not significant). Plasma insulin, glucagon, norepinephrine, and epinephrine concentrations were also similar in the two groups. In contrast, glucose Rd during exercise was 19% lower in the trained compared with the untrained subjects (27.0 +/- 2.6 vs. 33.2 +/- 1.5 mumol.min-1.kg-1; P < 0.001). Consequently, during exercise, plasma glucose concentration rose significantly (P < 0.05) in the trained subjects but did not change in the untrained subjects. We conclude that utilization of plasma glucose is lower in trained subjects during high-intensity exercise, even when the exercise is performed at the same relative (and therefore a higher absolute) intensity as in the untrained state. Hyperglycemia in trained subjects during intense exercise appears to be due to this lower rate of glucose utilization rather than a higher rate of glucose production.

Glucose-induced thermogenesis in postobese women who have undergone biliopancreatic diversion.

We evaluated the metabolic response to a standard (75-g) oral-glucose-tolerance test (OGTT) in eight post-obese women (PO) who underwent biliopancreatic diversion and in eight healthy control women (C). All subjects had been weight-stable for > or = 2 y. Blood samples for glucose, insulin, C-peptide, and nonesterified free fatty acids were taken at baseline and during 180 min after the glucose load. Plasma glucose and insulin concentrations at baseline and during the OGTT were similar in the two groups, suggesting the absence of an insulin-resistant state in the PO. Continuous indirect calorimetry was performed throughout the test. Glucose-induced thermogenesis (GIT) was higher in PO than in C (8.6 +/- 2.6 vs 4.3 +/- 1.9%; P < 0.01). These data indicate that GIT and insulin-glucose metabolism are not impaired in postobese patients when a near ideal body weight is reached and maintained after weight loss; this suggests that thermogenic deficiencies and hyperinsulinemia-insulin resistance are alterations secondary to obesity.