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Biomedical subjects

L Tappy

Publications and source records attributed to L Tappy.

At least 145 records · Page 8Linked to original sources
PubMed1988

Normalization of carbohydrate-induced thermogenesis by fructose in insulin-resistant states.

To examine whether defects in carbohydrate oxidation and thermogenesis in aging, obesity, and diabetes are secondary to impaired insulin action or to a primary defect in intracellular metabolism, we compared substrate oxidation and energy expenditure in 9 younger, 9 older, 9 obese, and 10 non-insulin-dependent diabetic subjects after the ingestion of 75 g of glucose or fructose (a monosaccharide whose transport into the cell and subsequent metabolism are independent of insulin). In young control subjects fructose produced a significantly greater increase in carbohydrate oxidation and energy expenditure than glucose despite significantly lower plasma glucose and insulin levels. In aged, obese, and diabetic individuals the increments in carbohydrate oxidation and energy expenditure after glucose ingestion were significantly imparied versus the younger controls. After fructose ingestion the increase in carbohydrate oxidation in the three insulin-resistant groups remained below that observed in the younger volunteers, whereas carbohydrate-induced thermogenesis was enhanced to levels that were comparable with those seen in the younger group. These data suggest that 1) the stimulation of thermogenesis after fructose ingestion is related to an augmentation of intracellular metabolism rather than an increase in the plasma insulin concentration per se, 2) the insulin resistance of aging, obesity, and diabetes is associated with a defect in intracellular carbohydrate oxidation, and 3) the cellular mechanisms involved in carbohydrate-induced thermogenesis are not primarily impaired in insulin-resistant states.

Blood Glucose↗
PubMed1988

Nonbinding inhibitory antiinsulin receptor antibodies. A new type of autoantibodies in human diabetes.

Sera and their IgG from 10/104 diabetic patients (five with insulin-dependent and five with noninsulin-dependent diabetes, NIDDM), contained antibodies that bound 125I-labeled purified human insulin receptors. 9 of these 10 sera failed to inhibit insulin binding (to rat hepatocytes and human placental membranes), did not stimulate glucose oxidation (by isolated rat adipocytes), and did not bind human placental IGF-1 receptors. Only one serum (and its IgG) modestly inhibited insulin binding and stimulated glucose oxidation. We conclude (a) that sera from 9/104 diabetics (five insulin-dependent and four noninsulin-dependent) contained a newly identified species of IgG antiinsulin receptor autoantibodies (AIRA), which bound to the insulin receptor at a locus different from the insulin binding site and did not inhibit insulin binding; and (b) that only 1/104 diabetic sera contained low-titer "conventional" antiinsulin receptor autoantibodies that bound to the insulin receptor at or near the insulin binding site, inhibited insulin binding and caused a clinical condition, which was difficult to distinguish from typical NIDDM.

Adolescent↗
PubMed1988

Antibodies to insulin-like growth factor I receptors in diabetes and other disorders.

A newly developed immunoprecipitation assay, with 125I-labeled highly purified human placental insulin-like growth factor I (IGF-I) receptor, was used to search for IGF-I-receptor antibodies in human sera. Eleven of 141 patient sera tested (7.8%) immunoprecipitated labeled IGF-I receptor. Immunoprecipitation was comparable with sera and IgG prepared from these sera. Seven of the 11 sera (3 of 31 with rheumatic disorders, 3 of 48 with non-insulin-dependent diabetes, and 1 of 52 with insulin-dependent diabetes) failed to inhibit IGF-I binding to human placental membranes and thus contained non-binding-inhibitory IGF-I-receptor antibodies. Their pathophysiological function remained uncertain. The remaining 4 sera (2 of 3 with type B severe insulin resistance, 1 of 7 with polycystic ovary syndrome (PCO), and 1 of 31 with rheumatic disorders) inhibited IGF-I binding. Plasma IGF-I concentrations were elevated (663 and 802 ng/ml, respectively) in 2 patients (1 with PCO and another with systemic lupus erythematosus) with binding-inhibitory IGF-I-receptor antibodies, suggesting IGF-I resistance that was probably mediated by the IGF-I-receptor antibodies. In conclusion, we identified two species of human IGF-I-receptor antibodies. Sera from 7 of 141 patients tested contained IgG autoantibodies that bound to the IGF-I receptor at a locus different from the IGF-I binding site and did not inhibit IGF-I binding. Sera from 4 of 141 patients contained antibodies that bound to the IGF-I receptor at or near the IGF-I binding site, inhibited IGF-I binding, and probably caused IGF-I resistance.

Adult↗
PubMed1988

Effect of hyperinsulinemia on urea pool size and substrate oxidation rates.

Recently, indirect calorimetry has frequently been used together with hyperinsulinemic clamps. With few exceptions, however, no attention was paid in these studies to the possible effects of hyperinsulinemia on urea nitrogen (N) pool size and the consequences of such changes on the calculated rates of protein, lipid, and carbohydrate (CHO) oxidation. We have determined the effects of euglycemic-hyperinsulinemic clamps on urea N pool size, urinary N excretion, and rates of protein, lipid, and CHO oxidation (measured by indirect calorimetry) in six normal men. Insulin infusion (1 mU.kg-1.min-1) increased peripheral venous insulin concentration from 7 +/- 1.2 (mean +/- SE) to 51 +/- 4 microU/ml. Glucose concentration was clamped at 84 +/- 1.1 mg/dl. Between 0 (preclamp) and 360 min (end of clamp), blood urea N concentration decreased from 17.2 +/- 1.1 to 11 +/- 0.8 mg/dl (P less than .001), and the urea N pool decreased from 604 +/- 41 to 388 +/- 30 mmol (P less than .001). The urea N production rate decreased from 461 +/- 91 (preclamp) to 91 +/- 63 mumol/min during the last 4 h of the clamp (P less than .05). Urinary N excretion remained unchanged (705 +/- 113 vs. 905 +/- 125 mumol/min, NS). Correction of urinary N excretion for insulin-induced reductions in the urea N pool resulted in the following changes in substrate oxidation rates (calculated for the last 4 h of the clamp).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Prevalence of thyroid disorders in psychogeriatric inpatients. A possible relationship of hypothyroidism with neurotic depression but not with dementia.

Thyroid disorders are known to manifest occasionally as isolated psychiatric disorders. In order to determine whether thyroid dysfunctions could play a significant role in the pathogenesis of psychiatric disorders in the elderly, the prevalence of thyroid disorders was compared in a group of psychogeriatric patients and in a group of nonpsychiatric elderly patients. Thyroid function screening was performed in 157 patients consecutively admitted to a psychogeriatric unit, and the prevalence of hypothyroidism was determined in the different groups of psychiatric disorders (senile and multi-infarct dementia, organic brain syndrome of other etiologies, psychotic depression, neurotic depression, chronic delusional state, acute confusional state, and personality disorder). Thyroid function screening was performed similarly in 104 unselected elderly patients admitted to the medico-surgical admission unit of the University hospital to assess the prevalence of hypothyroidism in a general, nonpsychiatric, elderly population. Eight patients were diagnosed as hypothyroid based on an elevated basal thyrotropin (TSH) and on thyrotropin-releasing hormone (TRH) test in the total number of patients, two in the nonpsychiatric and six in the psychiatric group. Three had clinical hypothyroidism, with decreased total and free T4 and T3 plasma levels in addition to increased basal TSH, five had biochemical hypothyroidism, with normal T4 and T3 levels and an excess TSH response to oral TRH. The prevalence of hypothyroidism in the two groups did not differ significantly (1.9% in the nonpsychiatric versus 3.8% in the psychiatric group). The prevalence of hypothyroidism in a subgroup of 88 patients with senile and multi-infarct dementia was 2.3%.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1986

Effect of alpha-glycohydrolase inhibitors (Bay m1099 and Bay o1248) on sucrose metabolism in normal men.

The inhibitory effect of N- beta-(4-ethoxycarbonylphenoxy-ethyl-1-desoxynojirimycin (BAY o1248) and of N-hydroxyethyl-1-desoxynojirimycin (BAY o1099) was studied in normal men. Nine healthy volunteers (weight range of 82% to 117% of their ideal body weight) ingested a 50 g sucrose load together with placebo, 50 mg BAY m1099, or 10 mg BAY of o1248. Their substrate oxidation rate was measured by continuous indirect calorimetry during four hours. The plasma glucose and plasma insulin peaks were both significantly blunted and the late fall of glycemia reduced. Mean plasma glucose, fructose, and insulin were reduced by both drugs during the first two hours following the sucrose load and led to a decrease of the suprabasal glucose oxidation (oxidation above baseline) during the first two hours of the test. However, the total suprabasal glucose oxidation during the four hours of the test was not significantly different from that of the control. Breath hydrogen, as an index of malabsorption, was shown to increase with both 50 mg BAY m1099 and 10 mg BAY o1248, starting from the third hour. These findings are consistent with a significant delay of sucrose absorption induced by these new alpha-glycohydrolase inhibitors.

1-Deoxynojirimycin↗
PubMed1986

Effects of cholinergic stimulation and antagonism on plasma insulin concentration in lean and obese human subjects.

The effect of cholinomimetic stimulation by infusion of edrophonium chloride or muscarinic blockade by infusion of atropine sulfate on insulin and GIP secretion was studied in normal lean subjects during eu- and hyperglycemia. Cholinomimetic stimulation led to a slight non-significant increase and muscarinic blockade to a slight, non-significant suppression of both GIP and insulin. No modification of the insulin secretion pattern was observed under either condition during hyperglycemia. The effect of atropine infusion on fasting plasma insulin and GIP was subsequently studied in 11 obese patients and 10 lean subjects. Muscarinic antagonism by atropine led to a transient non-significant suppression of GIP and insulin in lean subjects, but to a significant, sustained suppression of these hormones in obese patients. Insulin and GIP levels were however, not suppressed to control values after atropine administration in obese patients. A positive correlation was found between fasting plasma insulin and maximal suppression of insulin attained during the 30 min following administration of atropine. It is concluded that part of the hyperinsulinemia observed in human obesity is under the control of the parasympathetic nervous system. An abnormal balance between sympathetic inhibitory and parasympathetic stimulatory tones on insulin secretion, as observed in the VMH lesioned rat, might be present in human obesity.

Adult↗
PubMed1986

Metabolic effect of pre-cooked instant preparations of bean and potato in normal and in diabetic subjects.

The effect of a 50 g starch meal prepared with pre-cooked instant bean flakes on glucose and insulin plasma levels and on glucose oxidation rate as measured by continuous indirect calorimetry was assessed in six healthy human volunteers during 4 h following the meal. Comparison was done with the same load of starch as potato flakes to which the fiber and protein content of the bean meal had been added. Thirty minutes after ingestion, plasma glucose and insulin rise was less after beans than after potatoes (0.4 +/- 0.2 vs 2.0 +/- 0.3 mmol . l-1), p less than 0.01, and 8 +/- 2 vs 38 +/- 5 microU . ml-1, p less than 0.001). The elevation of glucose oxidation was markedly less during the 2 h following the ingestion of beans when compared to potatoes. The bean flakes meal gave rise to only moderate elevation of plasma glucose and insulin levels and of glucose oxidation rate when given to four noninsulin-dependent-diabetes mellitus patients. It is suggested that the slow carbohydrate property of legumes is not due to their fiber content, but might be related to the histological structure of the seed.

Adult↗
PubMed1986

Comparison of thermogenic effect of fructose and glucose in normal humans.

After nutrient ingestion there is an increase in energy expenditure that has been referred to as dietary-induced thermogenesis. In the present study we have employed indirect calorimetry to compare the increment in energy expenditure after the ingestion of 75 g of glucose or fructose in 17 healthy volunteers. During the 4 h after glucose ingestion the plasma insulin concentration increased by 33 +/- 4 microU/ml and this was associated with a significant increase in carbohydrate oxidation and decrement in lipid oxidation. Energy expenditure increased by 0.08 +/- 0.01 kcal/min. When fructose was ingested, the plasma insulin concentration increased by only 8 +/- 2 microU/ml vs. glucose. Nonetheless, the increments in carbohydrate oxidation and decrement in lipid oxidation were significantly greater than with glucose. The increment in energy expenditure was also greater with fructose. When the mean increment in plasma insulin concentration after fructose was reproduced using the insulin clamp technique, the increase in carbohydrate oxidation and decrement in lipid oxidation were markedly reduced compared with the fructose-ingestion study; energy expenditure failed to increase above basal levels. To examine the role of the adrenergic nervous system in fructose-induced thermogenesis, fructose ingestion was also performed during beta-adrenergic blockade with propranolol. The increase in energy expenditure during fructose plus propranolol was lower than with fructose ingestion alone. These results indicate that the stimulation of thermogenesis after carbohydrate ingestion is related to an augmentation of cellular metabolism and is not dependent on an increase in the plasma insulin concentration per se.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Insulin sensitivity and exogenous insulin clearance in Graves' disease. Measurement by the glucose clamp technique and continuous indirect calorimetry.

Insulin sensitivity was measured in a group of seven thyrotoxic patients and in a group of seven normal subjects by means of the glucose clamp technique. Infusion of insulin at a rate of 0.80 +/- 0.05 mU/kg X min in the hyperthyroid patients and of 0.55 +/- 0.04 mU/kg X min in the control group was performed to obtain a steady-state plasma insulin concentration of approximately 50 microU/ml. Substrate oxidation rates were measured in the postabsorptive state and during the 2 h of the clamp by means of continuous indirect calorimetry. In the postabsorptive state, hyperthyroid patients presented a preferential oxidation of lipids. During the period 60-120 min of the clamp, mean plasma glucose (92 +/- 2 versus 93 +/- 2 mg/dl), insulin (50 +/- 5 versus 58 +/- 3 microU/ml), and total glucose metabolism (5.8 +/- 0.7 versus 6.1 +/- 0.3 mg/kg X min) were similar in the hyperthyroid patients and the control subjects. The rate of glucose oxidation was higher in hyperthyroid patients than in control subjects (4.3 +/- 0.5 versus 2.2 +/- 0.2 mg/kg X min, P less than 0.001), while that of lipid oxidation was similar in both groups (0.6 +/- 0.2 versus control 0.7 +/- 0.1 mg/kg X min). The calculated metabolic clearance rate of insulin was markedly higher in the hyperthyroid patients (1144 +/- 132 ml/min) than in the normal subjects (812 +/- 56 ml/min, P less than 0.025). It is concluded that insulin sensitivity is not altered in the thyrotoxic state. The major route of insulin-stimulated glucose disposal in the hyperthyroid patients appears to be glucose oxidation.

Adult↗
PubMed1986

Effect of trestatin, a new inhibitor of pancreatic alpha-amylase, on starch metabolism in man.

The effect of two doses (3 mg and 10 mg) of the inhibitor of pancreatic alpha-amylase trestatin on the metabolism of an oral load of 75 g of starch was observed in healthy human subjects. The mean elevation of plasma glucose over the 4 h following the load was markedly reduced both with 10 mg (mean +/- s.e.m.: 1.4 +/- 1.2 mg/dl) and with 3 mg of trestatin (7.2 +/- 2.0 mg/dl) when compared to placebo (19.5 +/- 5.1 mg/dl) (P less than 0.01 in both cases). The mean elevation of plasma insulin was decreased with both 10 mg (mean +/- s.e.m.: 1 +/- 1 microU/ml) and 3 mg of trestatin (6 +/- 2 microU/ml) when compared to placebo (20 +/- 4 microU/ml) (P less than 0.01 in both cases). Suprabasal glucose oxidation, measured by indirect calorimetry, was markedly decreased by trestatin (mean +/- s.e.m.: 2.5 +/- 1.1 g/4 h with 10 mg of trestatin versus 12.0 +/- 2.0 g/4 h with placebo, P less than 0.001). To examine whether trestatin had any action on alpha-1-4 glycosidase activity, an oral load of 100 g sucrose together with either 50 mg trestatin or with a placebo was administered to four healthy human subjects. Trestatin was observed to have only few effects on plasma glucose and insulin levels following sucrose ingestion. This suggests that its main site of action is at the alpha-amylase level. Breath hydrogen was shown to increase after ingestion of starch plus trestatin at the two doses studied. It is concluded that trestatin is a powerful inhibitor of pancreatic alpha-amylase which could be of great help in the dietary management of diabetic patients.

Adult↗
PubMed1984

Effects of hypoxia and acidosis on vascular plasminogen activator release in the pig ear perfusion system.

The influence of hypoxia and acidosis on the release of vascular plasminogen activator was studied in the isolated perfused pig ear. Perfusion with deoxygenated or acid solutions led to significant increases in plasminogen activator release (p less than 0.001); acid solutions of pH 6.7 were more effective than those of pH 6.9. Perfusions with lactate and AMP, two metabolic products which might act as mediators of fibrinolytic stimulation during hypoxia, resulted in moderate increases of plasminogen activator in the effluent (p less than 0.01).

Acid-Base Equilibrium↗
PubMedDate not supplied

Hepatic de novo lipogenesis after liver transplantation.

BACKGROUND: The liver can synthesize fatty acids from carbohydrate (de novo lipogenesis [DNL]). We hypothesized that stimulation of this process may be involved in the development of obesity and dyslipidemia, 2 conditions frequently encountered after liver transplantation. METHODS: Hepatic fractional DNL and glucose metabolism were measured in 2 groups of 5 patients (age 36.8 +/- [SD] 14.9 years, BMI 26.3+/-5.3 kg/M2) 1 to 5 years after liver transplantation and 8 healthy subjects (age 28.1+/-5.3 years, BMI 27.2+/-4.5 kg/M2). Subjects were studied while receiving an isoenergetic nutrition (based on 1.1 x their basal energy expenditure) as hourly oral liquid formula during 10 hours. Their hepatic DNL was measured by infusing 1-13C acetate and measuring tracer incorporation in VLDL-palmitate. Their glucose metabolism was assessed by means of 6,6-2H2 glucose and indirect calorimetry. RESULTS: Two liver transplant recipients and 4 healthy subjects were obese, as defined by a BMI > 27 kg/M2. Fractional hepatic DNL was not different in the 2 groups of subjects: liver transplant recipients 3.1+/-1.7% vs 3.2+/-2.1% in healthy subjects. In both groups, DNL increased in proportion to BMI. When both groups were analyzed together, BMI was positively correlated with DNL (DNL = 0.28 x BMI - 4.28, r2 = .445, p < .05). Whole body glucose turnover was 15.0+/-4.4 micromol/kg per minute in liver transplant recipients and 15.8+/-4.1 micromol/kg per minute in healthy subjects (NS). Net carbohydrate oxidation tended to be lower in liver transplant recipients (8.1+/-2.6 micromol/kg per minute) than in healthy subjects (10.4+/-2.4 micromol/kg per minute; NS). Net nonoxidative glucose disposal (4.0+/-2.7 in liver transplant recipients vs 1.9+/-1.8 in healthy subjects, NS) and energy expenditure (0.065+/-0.01 vs 0.065+/-0.01 kJ/kg per minute) were similar in both groups. CONCLUSIONS: These results indicate that fractional hepatic DNL is not altered by liver transplantation during near continuous nutrition. The disposal of orally administered carbohydrate is also essentially unchanged. This strongly argues against a role of hepatic DNL in the pathogenesis of obesity and dyslipidemia after liver transplantation.

Adult↗
PubMedDate not supplied

Comparative study of maltitol and sucrose by means of continuous indirect calorimetry.

The metabolism of the hydrogenated disaccharide maltitol was compared to that of sucrose in a group of eight normal subjects. On two separate days, with an interval of at least one week each subject ingested a load of 30 g of either substance. The evolution of the levels of plasma glucose, insulin, and free fatty acids was followed during the 6 hr following the oral load. Carbohydrate and lipid oxidation rates were assessed simultaneously by continuous indirect calorimetry during the 6 hr following the oral load. Plasma glucose and insulin peaks occurred 30 min after ingestion of the load for both sugars. The peak of the delta glucose concentration was significantly smaller after maltitol than after sucrose (21 +/- 4 vs 38 +/- 4 mg/100 ml, p less than 0.02), as was the peak of the delta insulin concentration (9.3 +/- 2.7 microU/ml after maltitol vs 25.5 +/- 5.0 microU/ml after sucrose, p less than 0.001). The peak of the stimulation of glucose oxidation occurred 60 min after the load of sucrose and 90 min after the load of maltitol. The delta glucose oxidation was significantly lower with maltitol than with sucrose during the first 90 min after the ingestion of the load. It was slightly higher (although not significantly) with maltitol than with sucrose starting from the 210th min. Maltitol resulted in a cumulated suprabasal glucose oxidation which amounted to 40% that obtained with sucrose after 180 min.

Adult↗
PubMedDate not supplied

Energy balance in elderly patients after surgery for a femoral neck fracture.

To study energy and protein balances in elderly patients after surgery, spontaneous energy and protein intake and resting energy expenditure (REE) were measured in 20 elderly female patients with a femoral neck fracture (mean age 81 +/- 4, SD, range 74-87 years; weight 53 +/- 8, range 42-68 kg) during a 5-6 day period following surgery. REE, measured over 20-40 min by indirect calorimetry using a ventilated canopy, averaged 0.98 +/- 0.15 kcal/min on day 3 and decreased to 0.93 +/- 0.15 kcal/min on day 8-9 postsurgery (p less than 0.02). REE was positively correlated with body weight (r = 0.69, p less than 0.005). Mean REE extrapolated to 24 hr (24-REE) was 1283 +/- 194 kcal/day. Mean daily food energy intake measured over the 5-day follow-up period was 1097 +/- 333 kcal/day and was positively correlated with 24-REE (r = 0.50, p less than 0.05). Daily energy balance was -235 +/- 351 kcal/day on day 3 (p less than 0.01 vs zero) and -13 +/- 392 kcal/day on day 8-9 postsurgery (NS vs zero) with a mean over the study period of -185 +/- 289 kcal/day (p less than 0.01 vs zero). When an extra 100 kcal/day was allowed for the energy cost of physical activity, mean daily energy balance over the 5-day study period was calculated to be -285 +/- 289 kcal/day (p less than 0.01 vs zero). Measurements of total 24-hr urinary nitrogen (N) excretion were obtained in a subgroup of 14 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMedDate not supplied

Metabolic and respiratory effects of sodium lactate during short i.v. nutrition in critically ill patients.

BACKGROUND: Hyperglycemia and an increased ventilatory demand secondary to an increased CO2 production are frequent undesirable effects of total parenteral nutrition (TPN) in critically ill patients. This study was performed to assess whether sodium lactate as a metabolic substrate may affect these variables. METHODS: Five male patients with multiple trauma during the flow phase were studied during two consecutive 3-hour periods of isocaloric (1.1 x resting energy expenditure) TPN. Sixty-five percent of total calories was provided as carbohydrate, 15% as lipids, and 20% as amino acids during the first period (TPN-glucose), whereas 35% carbohydrate, 30% lactate, 20% lipids, and 15% amino acids (TPN-lactate) were substituted during the second period. Respiratory gas exchanges and net substrate oxidation were assessed by means of indirect calorimetry. Glucose kinetics was determined by primed-constant infusion of U-13C glucose. RESULTS: Compared with TPN-glucose, TPN-lactate decreased glycemia by 20%, insulinemia by 43%, net carbohydrate oxidation (assessed from indirect calorimetry) by 34%, and plasma glucose oxidation (assessed from 13CO2) by 54%. Respiratory oxygen exchange were increased by 3.7% due to a 20% thermic effect of lactate, but respiratory CO2 exchanges did not change. Pao2 decreased by 11.3 mm Hg, indicating that the increased O2 consumption was not matched by an appropriate increase in spontaneous ventilation. Arterial pH increased from 7.41 +/- 0.04 to 7.46 +/- 0.05. CONCLUSION: Sodium lactate as a metabolic substrate limits hyperglycemia but induces metabolic alkalosis and does not spare the ventilatory demand.

Adult↗
PubMedDate not supplied

Hepatic and peripheral glucose metabolism in intensive care patients receiving continuous high- or low-carbohydrate enteral nutrition.

BACKGROUND: The suppression of endogenous glucose production during parenteral nutrition is impaired in critically ill patients. It is, however, unknown whether enteral administration of carbohydrates, which normally promote hepatic glucose uptake, improves hepatic glucose metabolism in such patients. METHODS: We studied two groups of 7 patients during a 3-day continuous isocaloric enteral nutrition. A high-carbohydrate, low-lipid (EN-C) or a high-lipid, low-carbohydrate (EN-L) nutrient mixture was administered. RESULTS: Endogenous glucose production assessed with [2H7]glucose was similarly increased in both groups, indicating absence of its suppression by carbohydrate feeding. Gluconeogenesis estimated from [13C]glucose synthesis during [13C]bicarbonate infusion also was not suppressed by EN-C compared with EN-L. Systemic appearance of exogenous glucose was monitored by enteral infusion of [6,6-2H]glucose and was not different from the rate of glucose equivalent administered enterally, indicating no significant hepatic uptake of glucose in both groups. Plasma glucose and insulin concentrations were slightly higher with EN-C, although not significantly, and plasma triglycerides were similar in both groups. Both nutrition formulas were well tolerated clinically. CONCLUSIONS: These results indicate that enteral carbohydrate administration, whatever its quantity, fails to suppress endogenous glucose production and to promote net splanchnic glucose uptake in critically ill patients.

Adult↗