Biomedical subjects

P Arner

Publications and source records attributed to P Arner.

At least 199 records · Page 11Linked to original sources

PubMed1990

Acute effects of insulin-like growth factor I and insulin on glucose metabolism in vivo.

We have compared the actions of insulin-like growth factor (IGF-I) and insulin on glucose metabolism in vivo, using the glucose clamp technique in rats. Both hormones caused dose-dependent inhibition of hepatic glucose production, stimulation of whole body glucose disposal, and an increase in the glucose metabolic rate of specific muscles. Infusion of IGF-I also decreased the plasma concentration of insulin. An an infusion rate of 0.57 nmol.kg-1.min-1, IGF-I led to stimulation of whole body glucose uptake that was similar to the glucose uptake produced by infusion of 0.01 nmol.kg-1.min-1 insulin. The glucose metabolic rate, as measured by 2-deoxy-D-glucose uptake, was comparable in quadriceps femoris, soleus, and diaphragm muscles during the infusion of 0.57 nmol.kg-1.min-1 IGF-I and 0.01 nmol.kg-1.min-1 insulin. However, at these rates of infusion, IGF-I caused only a 38 +/- 6% inhibition of hepatic glucose output compared with 66 +/- 12% inhibition by insulin (P less than 0.05). Thus, under these conditions, muscle is more responsive than liver to IGF-I, which agrees with the complement of IGF-I receptors in the two tissues.

Animals↗

PubMed1990

Adrenergic regulation of lipolysis in situ at rest and during exercise.

The adrenergic regulation of lipolysis was investigated in situ at rest and during standardized bicycle exercise in nonobese healthy subjects, using microdialysis of the extracellular space in subcutaneous adipose tissue. The glycerol concentration was about two times greater in adipose tissue than in venous blood. At rest, the glycerol concentration in adipose tissue was rapidly increased by 100% (P less than 0.01) after the addition of phentolamine to the ingoing perfusate, whereas addition of propranolol did not alter the adipose tissue glycerol level. Glycerol in adipose tissue and plasma increased during exercise and decreased in the postexercise period. Propranolol in the perfusate almost completely inhibited the increase in the tissue dialysate glycerol during the exercise-postexercise period. Phentolamine, however, was completely ineffective in this respect. During exercise, the lipolytic activity was significantly more marked in abdominal than in gluteal adipose tissue; this was much more apparent in women than in men. Thus, in vivo lipolysis in subcutaneous adipose tissue is regulated by different adrenergic mechanisms at rest and during exercise. Alpha-adrenergic inhibitory effects modulate lipolysis at rest, whereas beta-adrenergic stimulatory effects modulate lipolysis during exercise. In addition, regional differences in lipolysis are present in vivo during exercise, which seem governed by factors relating to sex.

Adipose Tissue↗

PubMed1990

Catecholamine-induced lipolysis in adipose tissue of the elderly.

Age-dependent alterations in the effects of catecholamines on lipolysis were investigated in 25 young (21-35 yr) and 10 elderly (58-72 yr) healthy, nonobese subjects using isolated adipocytes obtained from abdominal subcutaneous tissue. Basal lipolysis was not affected by aging, while the rate of catecholamine-stimulated lipolysis was reduced by 50% in the elderly subjects (P less than 0.005). To elucidate the mechanisms behind this phenomenon lipolysis was stimulated with agents that act at well-defined steps in the lipolytic cascade, from the receptor down to the final step: the activation of the protein kinase/hormone-sensitive lipase complex. All agents stimulated lipolysis at a 50% lower rate in elderly as compared with young subjects (P less than 0.05 or less). However, half-maximum effective concentrations of the lipolytic agents were similar in both groups. The antilipolytic effects of alpha 2-adrenoceptor agonists were also the same in young and old subjects. Moreover, the stoichiometric properties of the beta- and alpha 2-receptors did not change with increasing age. In vivo studies performed on the same individuals likewise demonstrated an impaired lipolytic responsiveness, with 50% lower plasma glycerol concentrations during exercise in the elderly subjects (P less than 0.05), in spite of a normal rise in plasma norepinephrine. The plasma glycerol levels correlated strongly to the glycerol release caused by catecholamine-stimulated lipolysis in vitro in both young and elderly subjects (r = 0.8-0.9, P less than 0.001). In conclusion, a decreased activation of the hormone-sensitive lipase complex appears to be the mechanism underlying a blunted lipolytic response of fat cells to catecholamine stimulation in elderly subjects. This finding may, explain the age-dependent decreased lipolytic response to exercise in vivo.

Adipose Tissue↗

PubMed1990

Beta-adrenoceptor expression in human fat cells from different regions.

The expression of beta-adrenoceptors (BAR) was investigated in abdominal and gluteal fat cells of 32 nonobese men and women using radioligand binding and RNA excess solution hybridization. In both sexes the number of BAR binding sites was about twice as high in abdominal as in gluteal fat cells (P less than 0.01). Northern blot analysis of total RNA from adipose tissue showed hybridization of the BAR1 probe to an mRNA species of about 2.5 kb and of the BAR2 probe to an mRNA species of approximately 2.2 kb. The steady-state mRNA levels of BAR 1 and BAR 2 were also about twice as high in abdominal as in gluteal adipocytes of men and women (P less than 0.01). In abdominal fat cells the mRNA levels were approximately 45 and 30 molecules/cell for BAR1 and BAR2, respectively. There were no regional or sex variations in BAR 1 and BAR 2 mRNA stability. The apparent half-life of mRNA for both receptor subtypes was approximately 6 h in both regions. The mRNA levels for beta actin did not differ between the two regions in either sex. Thus, differences in expression of the genes encoding for BAR 1 and BAR 2 can explain why abdominal fat cells have more BAR than gluteal fat cells. This variation in gene expression may be a molecular mechanism underlying the well known regional differences in catecholamine-induced lipolysis activity between central and peripheral adipose tissue.

Adipose Tissue↗

PubMed1990

Glucocorticoid receptor messenger ribonucleic acid in different regions of human adipose tissue.

The expression of glucocorticoid receptor (GR) messenger RNA (mRNA) was investigated in sc adipose tissue and isolated adipocytes from the abdominal and gluteal regions in men and women using a human GR complementary RNA probe. GR mRNA levels were 2-fold higher in female than in male abdominal tissue or adipocytes, whereas in gluteal tissue or adipocytes no sex differences were observed. GR mRNA levels in female abdominal adipocytes were 50% higher than in corresponding female gluteal adipocytes; the opposite was observed corresponding in males. Northern blot analysis of total cellular RNA isolated from abdominal and gluteal adipocytes showed hybridization of the human GR probe to an RNA species of approximately 7.1 kilobases in both regions. No sex or regional differences in GR mRNA stability were observed. The human metallothionein II (hMTII) mRNA, which is regulated by glucocorticoids at the transcriptional level, showed an opposite sex and regional pattern as GR mRNA. However, in gluteal adipose tissue no sex differences were observed in hMTII mRNA levels. The expression of beta-actin mRNA, which is not regulated by glucocorticoids, showed no sex or regional variation. By immunocytochemistry, using an anti-GR-monoclonal antibody, cytoplasmic as well as nuclear staining for GR was demonstrated in both sexes and both regions. In conclusion, variations in GR mRNA levels between sexes and body regions may explain the well known sex and tissue differences in effects of glucocorticoids on human adipose tissue.

Abdomen↗

PubMed1990

Beta-adrenoreceptor subtype expression in human liver.

The pharmacological and gene expressions of beta 1- and beta 2-adrenoceptor subtypes (BAR1 and BAR2) were investigated in human liver by radioligand binding assays, adenylate cyclase experiments, and RNA excess solution hybridization. [125I]Cyanopinodolol, nonlabeled adrenergic agents, and BAR1/BAR2 cRNA were used as probes. The relationship between binding sites for BAR1 and BAR2 was markedly different from that between the basal mRNA expression for the two receptor subtypes. Plasma membranes as well as a microsomel-enriched fraction contained binding sites only for BAR2. The potency of BAR agonists and antagonists in stimulating adenylate cyclase activity of plasma membranes was typical of a BAR2 response. Northern blot analysis of total cellular RNA isolated from liver tissue showed hybridization of the BAR1 probe to a mRNA species of 2.5-2.6 kilobases and of the BAR2 probe to a mRNA species of 2.2-2.3 kilobases. The basal level of BAR1 mRNA was 5-fold higher than of BAR2 mRNA, as assayed by solution hybridization. No difference in BAR subtype mRNA stability was observed, as indicated by a mRNA half-life of approximately 5.5 h for both receptor subtypes. It is concluded that specific factors are involved in the steady state regulation of BAR subtype expression in human liver. This tissue contains solely BAR2 owing to a posttranscriptional block of basal BAR1 expression.

Adenylyl Cyclases↗

PubMed1990

In situ studies of catecholamine-induced lipolysis in human adipose tissue using microdialysis.

The effects of catecholamines on lipolysis in situ were investigated in humans. Subcutaneous adipose tissue was microdialyzed with solvents containing adrenergic agents. Norepinephrine caused a rapid increase in the glycerol level in adipose tissue (lipolysis index) that was further increased by the alpha adrenoreceptor blocker phentolamine. At 10(-11) mol/l of norepinephrine caused a 100% stimulation of lipolysis (P less than .025). In the presence of phentolamine the lipolytic effects of catecholamines at 10(-12) mol/l was isoproterenol greater than epinephrine greater than norepinephrine. All these three lipolytic catecholamines caused a transient increase in the adipose tissue dialysate glycerol level, which peaked after 20 to 30 min of catecholamine exposure and then declined. The apparent tachyphylaxia could not be overcome by a gradual increase of the catecholamine concentration from 10(-12) to 10(-8) mol/l. However, the selective alpha-2 adrenoreceptor agonist clonidine caused a continuous and dose-dependent decrease in the dialysate glycerol level; the minimum effective concentration was 10(-9) mol/l. In conclusion, catecholamines have a lipolytic effect in situ at much lower concentrations than those in the circulation. This effect is transient and is related to beta adrenoreceptors. In additio, catecholamines have alpha adrenoreceptor-mediated effects on lipolysis in situ.

Adipose Tissue↗

PubMed1989

Interactions between adenylate cyclase inhibitors and beta-adrenoceptors in isolated human fat cells.

Interactions between adenylate cyclase inhibitors and beta-adrenoceptors were investigated in isolated human fat cells. Phenylisopropyl adenosine, nicotinic acid and prostaglandine E2 induced a dose-dependent decrease in beta-adrenoceptor sensitivity; the concentration of isoprenaline causing half-maximum lipolytic effect increased 100-fold. The affinity constants for the high and low affinity beta-adrenoceptor states were increased 3000 and 700 times, respectively, but the total number of binding sites was unchanged. Pertussis toxin caused a dose-dependent increase of beta-adrenoceptor sensitivity to isoprenaline. There was a 200-fold increase in isoprenaline sensitivity in the lipolysis experiments and corresponding increases in the receptor affinity in the binding experiments. It is concluded that the affinity of human fat cell beta-adrenoceptors is reduced by adenylate cyclase inhibitors. This seems to be mediated by the Gi-protein and represents a new potential mechanism by which lipolysis is regulated by inhibitors of adenylate cyclase in man.

Adenylate Cyclase Toxin↗

PubMed1989

A new linear plot for standard curves in kinetic substrate assays extended above the Michaelis-Menten constant: application to a luminometric assay of glycerol.

In conventional kinetic substrate assays the standard curve is plotted as observed reaction rate, upsilon obs, versus added substrate concentration, Sadd, and has a linearity limited to Sadd much less than Km. From this plot the blank reaction rate, upsilon bl, is easily estimated but not the contaminating substrate concentration, Scon, present in reagents (unless it is the only blank source). Thus the actual substrate concentration, S = Scon + Sadd, cannot be estimated as required for the various linear plots based on the Michaelis-Menten equation. We have derived an expression, (upsilon obs - upsilon bl)/Vapp = Sadd/(Kmapp + Sadd), containing only those parameters measured for a conventional standard curve (Vapp and Kmapp are obtained from a plot of (upsilon obs - upsilon bl) versus (upsilon obs - upsilon bl)/Sadd). A plot of (upsilon obs - upsilon bl)/Vapp versus Sadd/(Kmapp + Sadd) can be used as a standard curve with the following advantages over the conventional standard curve: (a) For all kinetic substrate assays it is identical and connects the points (0, 0) and (1, 1). Thus deviations from true Michaelis-Menten kinetics or erroneous kinetic constants are easily detected. (b) Since it is linear even above Km, the analytically useful range is considerably extended. (c) For assays with a wide dynamic range it can be used in lin-lin or log-log form. The procedure is illustrated for a kinetic assay of glycerol (Kmapp = 40 mumol/liter). The plot was found to be entirely linear in the range 0.07-100 mumol/liter (glycerol concentration in cuvette).

Adenosine Triphosphate↗

PubMed1989

Automatic luminometric kinetic assay of glycerol for lipolysis studies.

A kinetic assay for glycerol based on the glycerokinase and firefly luciferin-luciferase reactions was developed for the purpose of allowing automatic analysis of large series of incubates from human fat cells. The method includes simplified sampled pretreatment and fully automated analysis, recording, and calculation of data. The upper limit of the dynamic range of the assay was extended from a glycerol concentration in cuvette of 2 up to 100 microM. This is due to a principally new method to linearize the nonlinear part of the standard curve. Recovery experiments reveal 100% glycerol recovery. Within-run and between-run precisions are high with coefficients of variation of between 1.2 and 3.7%. Samples are stable for up to 6 months in an ordinary freezer. The detection limit expressed as 2 SD of the blank result is 0.07 microM glycerol in cuvette, which is slightly lower when compared to the previous luminometric methods. The apparent blank, which is typically 0.4-1.0 microM glycerol in cuvette, has shown significant contributions only from bovine serum albumin, 0.03 microM, and glycerokinase, 0.01 microM. The analytical performance and degree of automation of the glycerol method described in this paper makes it well suited for serial studies of lipolysis in human fat cells in the presence of lipolytic or antilipolytic agents.

Adenosine Triphosphate↗

PubMed1989

Circulating insulin-like growth factor I in type 1 (insulin-dependent) diabetic patients with retinopathy.

The relationship between insulin-like growth factor I (IGF I) and diabetic retinopathy was investigated. This somatomedin circulates bound to at least two large carrier proteins with molecular weights of approximately 150,000 and 35,000. Total and protein binding profiles of insulin-like growth factor I were determined in the serum of 18 patients who had had Type 1 (insulin-dependent) diabetes for 15-20 years, but had no signs of nephropathy and a similar degree of mild subclinical neuropathy. Nine had preproliferative or proliferative retinopathy and 9 had little or no background retinopathy but there was no difference in diabetes duration, insulin doses or glycaemic control between the two groups. In the latter group, the amounts of the somatomedin I and the serum profiles were similar to those in 9 healthy control subjects. In patients with advanced retinopathy, however, binding of insulin-like growth factor I to the carrier proteins was significantly altered. Binding to the low molecular weight protein increased to 140% whereas binding to the large molecular weight protein decreased to 70% of the normal level. In the latter Type 1 diabetic patients total serum insulin-like growth factor I was decreased to 60% of the normal level (p less than 0.02). When the alteration in serum profile was adjusted for, the level of somatomedin associated with the small carrier complex was normal whereas that associated with the large carrier complex was reduced by almost 60% in Type 1 diabetic patients with retinopathy. It is proposed that the total circulating somatomedin level is low in advanced diabetic retinopathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Apparent lack of effect of obesity on the soluble phosphatidic acid phosphatase activity in human adipose tissue.

In view of previous reports that the activity of the Mg(++)-dependent phosphatidic acid phosphatase in adipose tissues of rat and mouse is elevated in obesity, we attempted to assay this activity in biopsies of human omental adipose tissue obtained from normal-weight and morbidly obese subjects in connection with operations. The major portion of the phosphatidic acid phosphatase activity was found in the cytosol, and the small amount found in the microsomal fraction was too low for accurate measurement. It was not possible to assay the activity in the crude cytosol. After precipitation with ammonium sulfate, however, the enzyme activity was linear with both the incubation time and the concentration of enzyme. It was not possible to obtain substrate saturation of the enzyme under the conditions employed. When assayed in the presence of a high concentration of substrate (0.6 mmol/l) the activity obtained in normal-weight patients, 7.8 +/- 2.4 nmol/mg protein/min (n = 10), was not significantly different from that in morbidly obese patients, 5.6 +/- 0.8 nmol/mg protein/min (n = 10). There was no relation between the size of adipose cells and phosphatidic acid phosphatase activity. Furthermore, there was no apparent relation between phosphatidic acid phosphatase activity in omental adipose tissue and that in the liver. The findings suggest that the increased biosynthesis of triglycerides in human obesity is not associated with an increased capacity of the soluble phosphatidic acid phosphatase in adipose tissue.

Adipose Tissue↗

PubMed1989

Microdialysis of subcutaneous adipose tissue in vivo for continuous glucose monitoring in man.

Subcutaneous adipose tissue extracellular glucose was investigated in vivo in man with a microdialysis technique. A small dialysis probe (4 or 10 x 0.5 mm) was implanted subcutaneously, and was perfused continuously with a micro-infusion pump. Dialysate samples were collected in 15-min periods. A transient yield of ATP was recorded immediately after insertion of the probe; thereafter ATP was almost undetectable. During steady-state conditions the tissue dialysate glucose concentration remained constant for at least 2 h, which indicated that there was no drainage of glucose from the interstitial fluid to the tissue dialysate. Simultaneous dialysis of venous blood and subcutaneous fat in rats showed that the recovery of glucose from the adipose tissue interstitial fluid to the dialysate was only 20% of that from blood. However, in vivo dialysis of human adipose tissue with glucose-containing solutions produced an equilibrium with the extracellular space at a glucose concentration that was similar to the blood glucose concentration. After oral glucose ingestion and following i.v. insulin and glucose administration the relative variations in subcutaneous glucose closely resembled those in blood glucose. It is concluded that the subcutaneous implantation of the presently used small dialysis device causes only minor and transient traumatic effects. The dialysis recovery of glucose is lower in adipose tissue than in blood. However, the relative kinetics of subcutaneous tissue dialysate glucose are closely related to variations in the blood glucose concentration, and thus may be used for monitoring of glycaemic control in man.

Adipose Tissue↗

PubMed1989

Mechanisms underlying regional differences in lipolysis in human adipose tissue.

Catecholamine-induced lipolysis was investigated in nonobese females and males. Isolated subcutaneous adipocytes were obtained from the abdominal and gluteal regions. The lipolytic effect of noradrenaline was four to fivefold more marked in abdominal adipocytes than in gluteal fat cells. This regional difference was more apparent in females than in males. No site differences were observed when lipolysis was stimulated with agents acting at different postreceptor levels. The beta-adrenergic lipolytic sensitivity was 10-20 times greater in abdominal adipocytes from both sexes than in gluteal adipocytes. Abdominal adipocytes from females showed a 40 times lower alpha 2-adrenergic antilipolytic sensitivity than did gluteal adipocytes, but the adenosine receptor sensitivity was similar in both sites. Beta-receptor affinity for agonists displayed no site or sex variation. Abdominal adipocytes showed a twofold increased beta-adrenoceptor density than did gluteal cells from both sexes. The alpha 2-adrenoceptor density was similar in all regions, but in females the affinity of clonidine for these sites was 10-15 times lower in the abdominal fat cells compared with gluteal cells. In conclusion, regional differences in catecholamine-induced lipolysis are regulated at the adrenoceptor level, chiefly because of site variations in beta-adrenoceptor density. Further variations in the affinity properties of alpha 2-adrenergic receptor in females may explain why the regional differences in catecholamine-induced lipolysis are more pronounced in women than in men.

Adipose Tissue↗

PubMed1989

Inhibition of lipolysis by agents acting via adenylate cyclase in fat cells from infants and adults.

The in vitro lipolytic effect of catecholamines is poor during infancy because of enhanced alpha 2-adrenoceptor activity. The mechanisms behind this were investigated in isolated fat cells obtained from 1- to 4-mo-old infants and from adults. The cells were incubated with agents that inhibit lipolysis through distinct receptors coupled to adenylate cyclase via the inhibitory GTP binding coupling protein, Gi. The sensitivity to the alpha 2-adrenoceptor agonist clonidine was 14 times higher in the infant group as compared to the adults, whereas that to an adenosine analogue was 14 times lower. The sensitivities to prostaglandin E2 and nicotinic acid were similar in both age groups. Preincubation of the adipocytes with pertussis toxin abolished the antilipolytic effects of all agents. The density of alpha 2-adrenoceptor binding sites determined with [3H]yohimbine was increased by about 25% in the infants. In conclusion, the antilipolytic sensitivity of adenosine and alpha 2-adrenoceptors develops separately and may play different roles in the regulation of lipolysis in man. Furthermore, the enhanced alpha 2-adrenoceptor sensitivity during infancy seems at least in part to be due to an increase in the number of receptors.

Adenylate Cyclase Toxin↗

PubMed1989

Abnormal action of catecholamines on lipolysis in adipocytes of type I diabetic patients treated with insulin.

Catecholamine-induced lipolysis was investigated in adipocytes obtained before and after 30 min of exercise from 10 insulin-treated type I (insulin-dependent) diabetic men and 10 male matched control subjects. The alpha 2-adrenoceptor-mediated antilipolytic effect of catecholamines was normal, but the beta-adrenoceptor-mediated lipolytic sensitivity was increased 10-fold (P less than .01) in diabetic subjects before and after exercise. The latter correlated inversely (r greater than .7) with the circulating norepinephrine level, which was significantly reduced in diabetic subjects. Basal lipolysis and lipolysis activated at different steps distal to the beta-receptor were similar in the two groups. There was no major change in the total number of beta- and alpha-adrenoceptors in the diabetic patients. However, the proportion of high-affinity beta-adrenoceptors was significantly increased in these patients compared with control subjects. In the diabetic patients, approximately 50% of the beta-adrenoceptors were in a high-affinity state, compared to approximately 30% in the control subjects (P less than .025). In diabetic subjects there was an enhanced plasma glycerol response to exercise, despite a blunted plasma norepinephrine response. The data suggest enhanced sensitivity of catecholamine-induced lipolysis in type I diabetes due to an increase in the number of high-affinity (i.e., coupled) beta-adrenoceptors in fat cells. This mechanism may be due to low levels of circulating norepinephrine and may also explain the exaggerated lipolytic response to exercise in the diabetic state.

Adipose Tissue↗

PubMed1989

Antilipolytic effects of insulin and adenylate cyclase inhibitors on isolated human fat cells.

Antilipolysis induced by insulin by adenylate cyclase inhibitors was compared in isolated human fat cells when lipolysis was activated at well-defined steps in the cyclic AMP system. The latter was achieved with isoprenaline (beta-adrenoreceptor agonist), cholera toxin and pertussis toxin (acting on the GTP-sensitive coupling proteins), forskolin (stimulating the catalytic component of adenylate cyclase), enprofylline (selective phosphodiesterase inhibitor) and N6-monobutyryl-cyclic-AMP or 8-bromo cyclic-AMP (cyclic AMP analogues which are resistant or sensitive to phosphodiesterase, respectively). Clonidine (alpha 2-adrenoreceptor agonist), prostaglandin E2 and N6-(phenylisopropyl) adenosine (adenosine analogue) failed to inhibit lipolysis stimulated by cholera toxin or pertussis toxin, but were effective under all other conditions. Insulin failed to inhibit lipolysis stimulated by enprofylline or N6-monobutyryl cyclic AMP, but was effective under all other circumstances. In conclusion, insulin and adenylate cyclase inhibitors are antilipolytic in human fat cells through different mechanisms. Adenylate cyclase inhibitors act predominantly on the GTP-sensitive coupling proteins and, to a minor extent, at some yet unidentified distal step in the lipolytic machinery. As regards insulin, the major site of the antilipolytic action is phosphodiesterase.

Adenylyl Cyclase Inhibitors↗

PubMed1989

Characterization of insulin resistance after surgery.

The effects of insulin on glucose utilization were investigated in seven nonobese patients before and 24 hours after elective cholecystectomy. Surgery was followed by a significant increase in the circulating levels of glucose and insulin. The hypoglycemic action of insulin was reduced by one third (p less than 0.01) after surgery. In isolated fat cells after surgery there was a significant overall reduction of 35% to 50% of the effects of insulin on 3-0-methylglucose transport and lipogenesis at 1 mumol/L of glucose (where hexose transport is rate-limiting for insulin action). However, there was no change in insulin sensitivity in these cells. The effects of insulin on lipogenesis in adipocytes incubated with 100 mumol/L of glucose (where glucose metabolism is rate-limiting for insulin action) and adipocyte insulin receptor binding were not influenced by surgery. Insulin action in vivo and in vitro was not altered in five nonoperated control subjects 24 hours after they were given the same type of nutritional support as the cholecystectomy patients postoperatively. It was concluded that an elective moderate surgical trauma induces a rapid and marked insulin resistance that is not the result of postoperative nutritional restriction and involves a postreceptor binding alteration of glucose transport.

3-O-Methylglucose↗