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PubMed1993

Regulation of intestinal proglucagon-derived peptide secretion by glucose-dependent insulinotropic peptide in a novel enteroendocrine loop.

Incretins are intestinal factors that stimulate postprandial insulin secretion in preparation for subsequent rises in plasma levels of ingested nutrients. Glucose-dependent insulinotropic peptide (GIP), a duodenal endocrine peptide, is ideally located for such a function. In contrast, the intestinal proglucagon-derived peptide (PGDP), truncated GLP-1 [GLP-1(7-37) or tGLP-1] is equipotent to GIP in insulinotropic activity, but due to its localization in the distal ileum, appears to be poorly situated to fulfill an incretin role in response to direct nutrient stimulation. Despite its distribution, rapid increments in plasma levels of tGLP-1 have been noted in response to nutrient ingestion. We have recently reported that GIP (but not other nutrient-stimulated duodenal endocrine peptides) can stimulate intestinal PGDP secretion in vitro, and therefore hypothesized that GIP might regulate secretion of the intestinal PGDPs, including tGLP-1, in response to nutrient ingestion in vivo in the rat. Placement of either fat or glucose directly into the ileal lumen was demonstrated to significantly stimulate secretion of the intestinal PGDPs (P < 0.05), whereas fat or glucose in the duodenal lumen significantly increased plasma levels of GIP (P < 0.05). In addition, however, duodenal fat treatment also increased the secretion of intestinal PGDPs into the circulation (P < 0.05), with levels rising to same extent as observed after direct administration of fat into the ileum. The rise in plasma GIP levels in response to duodenal fat treatment occurred slightly before the increments in intestinal PGDP levels, suggesting a relationship between the two peptides. Intravenous infusion of GIP to give concentrations similar to those observed after duodenal fat administration induced a 2-fold increase in plasma levels of intestinal PGDPs that was independent of glycemic levels (P < 0.05). No increment in intestinal PGDPs was found in response to infusion of another duodenal endocrine peptide, cholecystokinin. Thus, these data demonstrate a specific effect of GIP to stimulate secretion of the intestinal PGDPs in vivo in the rat. This enteroendocrine loop between the duodenal peptide GIP and the ileal PGDPs may account for some of the early rises in secretion of tGLP-1 observed in response to nutrient ingestion.

Animals↗

PubMed1990

Involvement of alpha-2 adrenergic receptor subtypes in hyperglycemia.

Alpha-2 adrenoceptor stimulation induces in the mouse a hyperglycemic response which is accompanied by a concomitant inhibition of insulin secretion. To test the possibility that one of the postulated subtypes of alpha-2 adrenoceptors is preferentially implicated in this response, we compared the interaction of several drugs with known selectivity toward alpha-2A or alpha-2B adrenoceptor subtypes in our model. The alpha-2A preferential agonist oxymetazoline induced in the mouse a hyperglycemic response similar to that of the nonselective alpha-2 adrenoceptor agonist UK 14.304. This hyperglycemic response to oxymetazoline was accompanied by a concomitant inhibition of insulin release. Both the effect on glycemic level and the inhibition of insulin release by oxymetazoline were antagonized by the alpha-2 adrenoceptor antagonist idazoxan. The alpha-2B preferential antagonists ARC-239, prazosin or chlorpromazine failed to block the modifications in both glycemic and insulin levels induced by alpha-2 adrenoceptor stimulation. The nonselective antagonists rauwolscine, yohimbine, WY 26703, phentolamine and corynanthine, as well as the receptor antagonists with alpha-2A selectivity like WB 4101, idazoxan and tolazoline, dose-dependently antagonized both the glycemic and the insulin responses to UK 14.304. A positive correlation was obtained between the potencies of these drugs in antagonizing the hyperglycemic response to UK 14.304 and their affinities for alpha-2A adrenergic receptors (r = 0.918, P less than .001) but no correlation was obtained with their affinities for alpha-2B adrenergic receptors (r = 0.048, P = N.S.)(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗

PubMedDate not supplied

Reduction in blood and urine glucose levels in streptozotocin and alloxan diabetes by phenazine methosulfate.

The purpose of this investigation was to ascertain the ability of phenazine methosulfate (PMS) to improve the streptozotocin (STZ) and alloxan induced diabetic condition in vivo as determined by changes in blood and urine glucose levels and by alteration in the secretion of insulin by isolated islets. STZ and alloxan diabetes was induced in male albino rats (200-250 g body weight). A single injection of PMS (6.0 mg/kg) or nicotinamide (500 mg/kg) simultaneously with diabetic doses of either STZ or alloxan caused a significant reduction in blood and urine glucose levels three days after the injection. The reduction in glycemic levels was greater with PMS than with nicotinamide. Daily PMS (0.5 mg/kg) injection, initiated 5, 10, 20 or 30 days after the development of STZ- and alloxan-diabetes, caused a significant decrease in blood and urine glucose levels and also increased body weight determined 60 days after STZ or alloxan administration. These effects were observed even if the injections were initiated 20 or 30 days after the onset of the diabetic syndrome. Glucose stimulated insulin secretion was significantly inhibited by pre-incubation of isolated islets for one hour at 37 degrees C with either STZ or alloxan. However, insulin secretion was induced by PMS in the STZ or alloxan pretreated islets. Nicotinamide neither protected nor induced insulin secretion under similar conditions. The level of insulin secretion induced by PMS whether in the normal islets or in islets previously exposed to the B-cytotoxic agents were comparable in quantity to glucose (17 mM)-stimulated insulin secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Changes in cortical functioning with acute hypoglycemia and hyperglycemia in type I diabetes.

In this study, 18 type I (insulin-dependent) diabetic subjects aged 22-35 yr (mean age 29.3) and within 10 yr of diagnosis (mean 7.7) performed a battery of cognitive and psychomotor tasks under conditions of hypoglycemia (50 mg/dl), normoglycemia (100 mg/dl), and hyperglycemia (300 mg/dl). Blood glucose levels during testing were precisely maintained at the preselected level via a Biostator insulin/glucose-infusion system. The order of glycemic level was counterbalanced across subjects in a single-blinded design. Performance on tasks requiring visual tracking, visuomotor speed, concentration, and planning ability (pursuit rotor and trails B) were significantly impaired under conditions of hypoglycemia compared with normoglycemic levels. Visual reaction time was not significantly impaired under conditions of hypoglycemia or hyperglycemia.

Adolescent↗

PubMed1999

Transcutaneous glucose measurement using near-infrared spectroscopy during hypoglycemia.

OBJECTIVE: To analyze a transcutaneous near-infrared spectroscopy system as a technique for in vivo noninvasive blood glucose monitoring during euglycemia and hypoglycemia. RESEARCH DESIGN AND METHODS: Ten nondiabetic subjects and two patients with type 1 diabetes were examined in a total of 27 studies. In each study, the subject's plasma glucose was lowered to a hypoglycemia level (approximately 55 mg/dl) followed by recovery to a glycemic level of approximately 115 mg/dl using an intravenous infusion of insulin and 20% dextrose. Plasma glucose levels were determined at 5-min intervals by standard glucose oxidase method and simultaneously by a near-infrared spectroscopic system. The plasma glucose measured by the standard method was used to create a calibration model that could predict glucose levels from the near-infrared spectral data. The two data sets were correlated during the decline and recovery in plasma glucose, within 10 mg/dl plasma glucose ranges, and were examined using the Clarke Error Grid Analysis. RESULTS: Two sets of 1,704 plasma glucose determinations were examined. The near-infrared predictions during the fall and recovery in plasma glucose were highly correlated (r = 0.96 and 0.95, respectively). When analyzed during 10 mg/dl plasma glucose segments, the mean absolute difference between the near-infrared spectroscopy method and the chemometric reference ranged from 3.3 to 4.4 mg/dl in the nondiabetic subjects and from 2.6 to 3.8 mg/dl in the patients with type 1 diabetes. Using the Error Grid Analysis, 97.7% of all the near-infrared predictions were assigned to the A-zone. CONCLUSIONS: Our findings suggest that the near-infrared spectroscopy method can accurately predict plasma glucose levels during euglycemia and hypoglycemia in humans.

Adult↗

PubMed2000

Portal glucose infusion in the mouse induces hypoglycemia: evidence that the hepatoportal glucose sensor stimulates glucose utilization.

To analyze the role of the murine hepatoportal glucose sensor in the control of whole-body glucose metabolism, we infused glucose at a rate corresponding to the endogenous glucose production rate through the portal vein of conscious mice (Po-mice) that were fasted for 6 h. Mice infused with glucose at the same rate through the femoral vein (Fe-mice) and mice infused with a saline solution (Sal-mice) were used as controls. In Po-mice, hypoglycemia progressively developed until glucose levels dropped to a nadir of 2.3 +/- 0.1 mmol/l, whereas in Fe-mice, glycemia rapidly and transiently developed, and glucose levels increased to 7.7 +/- 0.6 mmol/l before progressively returning to fasting glycemic levels. Plasma insulin levels were similar in both Po- and Fe-mice during and at the end of the infusion periods (21.2 +/- 2.2 vs. 25.7 +/- 0.9 microU/ml, respectively, at 180 min of infusion). The whole-body glucose turnover rate was significantly higher in Po-mice than in Fe-mice (45.9 +/- 3.8 vs. 37.7 +/- 2.0 mg x kg(-1) x min)-1), respectively) and in Sal-mice (24.4 +/- 1.8 mg x kg(-1) x min(-1)). Somatostatin co-infusion with glucose in Po-mice prevented hypoglycemia without modifying the plasma insulin profile. Finally, tissue glucose clearance, which was determined after injecting 14C-2-deoxyglucose, increased to a higher level in Po-mice versus Fe-mice in the heart, brown adipose tissue, and the soleus muscle. Our data show that stimulation of the hepatoportal glucose sensor induced hypoglycemia and increased glucose utilization by a combination of insulin-dependent and insulin-independent or -sensitizing mechanisms. Furthermore, activation of the glucose sensor and/or transmission of its signal to target tissues can be blocked by somatostatin.

Animals↗

PubMed1999

Glucose-dependent stimulatory effect of glucagon-like peptide 1(7-36) amide on the electrical activity of pancreatic beta-cells recorded in vivo.

The stimulatory effect of the glucagon-like peptide (GLP)-1(7-36) amide on electrical activity in pancreatic b-cells recorded in vivo was studied. The injection of GLP-1 produces a lengthening of the active phase with respect to the silent phase, leading to a stimulation of insulin release, which produces a secondary decrease in blood glucose concentration and eventually, to the hyperpolarization of the membrane at a blood glucose level of approximately 5 mmol/l. The injection of GLP-1 at a glycemic level <5 mmol/l does not stimulate electrical activity. This is in contrast to the effect of tolbutamide, which stimulates electrical activity at low glucose concentrations. These results demonstrate that in vivo, the stimulatory effect of GLP-1 on insulin secretion is at least partially mediated by its effect on beta-cell electrical activity. Furthermore, the glucose dependence of the effect confers to GLP-1, a security factor that supports its potential use in the treatment of type 2 diabetes.

Animals↗

PubMedDate not supplied

Role of self-monitoring of blood glucose in glycemic control.

OBJECTIVE: To examine the role of self-monitoring of blood glucose (SMBG) in the management of diabetes mellitus. METHODS: Current trends and published evidence are reviewed. RESULTS: Despite the widespread evidence that lowering glycemic levels reduces the risks of complications in patients with diabetes, little improvement in glycemic control has been noted among patients in the United States and Europe in recent years. Although SMBG has been widely used, considerable controversy surrounds its role in achieving glycemic control. The high cost of test strips has made considerations regarding appropriate recommendations for SMBG a priority, especially in light of the current climate of health-care cost-containment. Existing clinical recommendations lack specific guidance to patients and clinicians regarding SMBG practice intensity and frequency, particularly for those patients not treated with insulin. Previous studies of the association between SMBG and glycemic control often found weak and conflicting results. CONCLUSION: A reexamination of the role of SMBG is needed, with special attention to the unique needs of patients using different diabetes treatments, within special clinical subpopulations, and during initiation of SMBG versus its ongoing use. Further understanding of the intensity and frequency of SMBG needed to reflect the variability in glycemic patterns would facilitate more specific guideline development. Educational programs that focus on teaching patients the recommended SMBG practice, specific glycemic targets, and appropriate responses to various blood glucose readings would be beneficial. Continuing medical education programs for health-care providers should suggest ways to analyze patient SMBG records to tailor medication regimens. For transfer or communication of SMBG reports to the clinical staff, a standardized format that extracts key data elements and allows quick review by health-care providers would be useful. Because the practice of SMBG is expensive, the cost-effectiveness of SMBG needs to be carefully assessed.

Blood Glucose↗

PubMed2000

[How to measure glycemic instability?].

Instability of glycemic levels is "normal" in type 1 diabetes, with different levels of severity, up to the restrictive definition of brittle diabetes (repeated ketoacidosis and/or severe hypoglycemias). Quantification of glycemic instability, in terms of intraday variability and day-to-day reproducibility, is advisable. Standard deviation of blood glucose, though a simple index does not discriminate between slow and brutal variations. Repartition of blood glucose values also only indicates dispersion. M values compares the patient values to an ideal blood glucose level, emphasizing the role of low values. The MAGE index measures the amplitude of the largest glucose excursions, thus evaluating appropriately glycemic variability. The Low Blood Glucose Index (LBGI) is a new index of variability emphasising (as the M value) the low glycemias. Each glycemia is given a value from O (if >=110 mg/dl) to 100 (if 20 mg/dl). It thus integrates the frequency and severity of hypoglycemias. According to its authors the LBGI would be the best indicator of severe hypoglycemias. The Mean of Daily Differences (MODD) evaluates the day-to-day reproducibility of blood glucose values. All the above indexes could easily be incorporated in the programmes of large memory glucose meters.

Blood Glucose↗

PubMed1989

Autoantibodies to the insulin receptor impair clearance of plasma endogenous insulin.

Plasma insulin clearance was studied in a patient with autoantibodies to the insulin receptor, manifesting persistent hyperinsulinemia associated with alternating hyper- and hypoglycemia. In the postabsorptive period, the plasma glucose level gradually decreased. To prevent the development of hypoglycemia, glucose was infused and the glycemic level was clamped at 50 mg/dl without insulin infusion. The plasma C-peptide level was below the detectable range during the clamp, indicating no appreciable secretion of insulin. The plasma insulin level declined exponentially with a markedly prolonged disappearance rate (half-time: 3.0 h) during the study. These results indicate that hyperinsulinemia in the postabsorptive period in this patient is attributable to the impairment of plasma insulin clearance through receptor-mediated mechanisms, and also confirm that the receptor plays the principal role in plasma insulin removal.

Acanthosis Nigricans↗

PubMed1995

A selective decrease in the beta cell mass of human islets transplanted into diabetic nude mice.

Streptozocin-induced diabetic nude mice (blood glucose 493 +/- 14 mg/dl) received aliquots of 2000 human islet equivalents (IE) under the kidney capsule and were then followed for up to 30 days with measurement of blood glucose concentration and body weight. Characterization of islet aliquots before the implantation included the assessment of the endocrine beta cell and nonbeta cell mass, estimated by point counting morphometry of immunostained sections. Islet transplantation was followed by a rapid decrease in blood glucose levels and by a progressive increase in body weight; 15 days after transplantation mean glycemic levels were 102 +/- 11 mg/dl and further decreased to 70 +/- 3 mg/dl at 30 days. Despite the progressive improvement in the glucose levels, the beta cell mass of the islet grafts significantly decreased over time from 2.63 +/- 0.2 mg, at the time of transplantation, to 1.16 +/- 0.1 and 0.86 +/- 0.1 mg 15 and 30 days, respectively, after transplantation. In contrast, the endocrine nonbeta cell mass remained stable from before the implantation to 30 days after. Therefore, the endocrine nonbeta cell/beta cell ratio increased from 14% at the time of transplantation, to 35% and 37%, 15 and 30 days, respectively, after transplantation. The rate of replication of the transplanted beta cells was similar in the grafts harvested at 15 and 30 days, with the percentage of beta cells positive for bromo-2' deoxyuridine (BrdU) incorporation being in the range of approximately 0.1% 6 hr after the BrdU injection. These data demonstrate that an important decrease in beta cell mass takes place immediately after islet transplantation--the most dramatic decrease occurring in the first 15 days and persisting even after revascularization has occurred. However, endocrine nonbeta cell mass remained stable indicating that engrafted nonbeta cells are less likely to die than beta cells. The finding that the nonbeta/beta cell ratio of a human islet graft can increase over time, raises questions about whether such a change in islet structure could have an influence upon function.

Animals↗

PubMed1993

Naloxone effects on post-prandial glucose, insulin and C-peptide levels in obese subjects.

In order to investigate the relationships between glucose metabolism, insulin secretion and endogenous opioids in obese patients, we have studied the effects of a naloxone infusion on insulin and C-peptide release after a normal meal (800 kcal) eaten at 12.00 hr in 16 obese women, aged 20-61 yr, with a BMI ranging from 25 to 37.2 kg/m2, with normal glucose tolerance (Group 1) and with NIDDM (Group 2). Naloxone was administered in a bolus of 1.6 mg i.v., followed by a continuous infusion of 4 mg in 2 hr starting immediately after feeding. In Group 1 naloxone infusion significantly increased the glucose levels, but insulin secretion was unaffected. In Group 2, naloxone infusion failed to modify significantly the postprandial levels of glucose, insulin and C-peptide. Therefore, in our study naloxone infusion seems to have beta-endorphin-like effects in non-diabetic obese subjects by increasing their glycemic levels, with no evidence of expected insulin decrease. In diabetic obese patients we observed a trend towards decrease in glycemic values during naloxone infusion, as expected, due to insulin plasma levels increase. By these data we can hypothesise a complex regulatory role of opioids in metabolic balance in obesity. In diabetic patients, naloxone can improve the surviving insulin secretion with better glucose tolerance. In non-diabetic subjects naloxone exerts its effects, probably, on peripheral organs.

Adult↗

PubMed1976

Glucose-insulin metabolism in chronic schizophrenia.

The present study deals with possible connections between the schizophrenic syndrome and alterations of the glucose-insulin metabolism. Data have been obtained in 18 patients, 9 males and 9 females, aged 22-62 years, suffering from chronic schizophrenia of 5-29 years duration. The patients were treated with Haloperidol for 30 days, 6 mg, i.m.p.d. to a total dose of 180 mg. The glucose metabolism was examined through a GTT (with a glucose load of 100 gr. per os), and an Insulin Tolerance Test (with 0.1 U/kg body weight). The insulin levels were examined under glucose load by the radioimmunological assay of Hales and Randle. The glycemic levels were examined under glucose load by an oxidative method. The psychopathological features were controlled by a Wittenborn Rating Scale. The metabolic and psychological examinations were done twice before the beginning of therapy, at 46 hrs. interval, then at 10-20-30 days of therapy. The results are probative for the presence of a chemical diabetes in a significantly high percent of patients. The significance of possible neurotransmitter impairments acting at both the biochemical and psychological levels is discussed.

Adult↗

PubMed2005

Effect of diabetes drug counseling by pharmacist, diabetic disease booklet and special medication containers on glycemic control of type 2 diabetes mellitus: a randomized controlled trial.

BACKGROUND: type 2 diabetes mellitus continues to increase in prevalence worldwide. Many factors have been cited as contributing to compliance, such as family and social support, education, number of tablets per dose, frequency of administration and health care provider communication. Toward these goals, the present study was developed to measure the effect offactors on glycemic control such as diabetes education by pharmacists, a diabetes disease booklet and special medication containers. MATERIAL AND METHOD: A total of 360 volunteers with type 2 DM patients were recruited, participants were simple randomized to control 180 and intervention 180 patients. Which intervention categorized to 4 groups; all intervention groups received diabetes drug counseling by a pharmacist, one group received plus a diabetes booklet, one received plus special medical containers and the last group received all of them. The interventions were done at the 1st time of visit. Both the control and intervention groups were monitored for fasting plasma glucose and HbA1c at 0, 3, 6 months and glycemic level in both groups was compared. RESULTS: After 3 months, mean fasting plasma glucose and HbA1c decreased wiih the intervention group vs. control group (152.36 +/- 39.73 to 131.52 +/- 35.22 mg%) and (150.16 +/- 41.78 to 153.98 +/- 47.95 mg%) respectively; (p < 0.001). HbA1c level 8.16 +/- 1.44 to 7.72 +/- 1.26 vs 8.01 +/- 1.51 to 8.38 +/- 1.46 respectively; (p < 0.001). After 6 months, mean fasting plasma glucose and HbA1c decreased with the intervention group vs. control group (152.36 +/- 39.73 to 145.20 +/- 46.07 mg%) and (150.16 +/- 41.78 to 159.16 +/- 54.90 mg%) respectively; (p < 0.013). HbA1c level 8.16 +/- 1.44 to 7.91 +/- 1.27 vs. 8.01 +/- 1.51 to 8.80 +/- 1.36 respectively; (p < 0.001). The most favorable glycemic outcome was the group that received all of the interventions; mean FPG was reduced from 147.46 +/- 36.07 to 125.38 +/- 31.12 mg% (p < 0.000) in 1nd visit (3 months later) and still reducing effect on the 2nd visit (6 month later) mean FPG from 147.46 +/- 36.07 to 130.21 +/- 33.96 mg% (p < 0.016) also the same way in HbA 1c level. The group that received only drug counseling by pharmacist had no significant reduction in FPG and HbA1c. (p > 0.05). CONCLUSION: Drug counseling by a pharmacist has little beneficial effect on diabetes management outcome compared to the diabetes booklet and special drug container. To improve glycemic control of type 2 DM is to integrate self-management in daily life, wide a variety of education, drug taken behavior and health care provider available communication produce improvement in patient management and is somewhat better when used in combination.

Adult↗

PubMed1978

[Low doses of insulin--comparison between hyperosmolar nonketotic coma and diabetic ketoacidosis (author's transl)].

The authors present a comparison between the results achieved in the treatment of 11 cases of nonketotic hyperosmolar "coma" and 13 cases of diabetic ketoacidosis using low doses of intramuscular insulin hourly. Surprisingly both, larger amounts of insulin and longer periods were needed to compensate the metabolic disturbance of the nonketotic hyperosmolar "coma" cases when compared to the ketoacidosis ones. The data obtained in this study suggest a possible direct relationship between the initial urea levels and the total amount of insulin needed to reduce the initial glycemia to a normal glycemic level.

Adult↗

PubMedDate not supplied

What is the proper use of hemoglobin A1c monitoring in the elderly?

Diabetes mellitus (DM) is a major health problem for the aging population. Glycemic control is fundamental to the management of diabetes, as glycemic levels are closely linked to development of diabetes-related complications. Measurement of the hemoglobin A1c (A1c) to assess chronic glycemic control is an integral component of diabetes care. Currently, there is no clear evidence that age alters the relationship between A1c and average blood glucose. The Diabetes Control and Complications trial and the United Kingdom Prospective Diabetes Study are the 2 main studies that have provided evidence leading to the widespread recommendation of A1c monitoring. The American Diabetes Association recommends achieving an A1c level of 7% or lower. However, older diabetics represent a heterogeneous population ranging from frail nursing home residents to active community-dwelling elderly with variable life expectancies. One needs to look at the individual in order to best balance risk versus benefit associated with tight glycemic control. Benefits of intensive therapy in an effort to lower A1c must always be weighed against the greater risk of disabling and unpredictable hypoglycemia, as the geriatric population is less likely to benefit from reducing the risk of microvascular complications and more likely to suffer serious adverse effects from hypoglycemia.

Age Factors↗

PubMed2006

What is the proper use of hemoglobin A1c monitoring in the elderly?

Journal Article↗

PubMed2003

Comparison of a high-protein disease-specific enteral formula with a high-protein enteral formula in hyperglycemic critically ill patients.

AIMS: To determine whether a specific high-protein enteral formula with a similar caloric percentage of fat and carbohydrates achieves greater control over glycemic levels and reduces insulin requirements in hyperglycemic critically ill patients when compared to a control high-protein enteral formula. DESIGN: A prospective, randomized, controlled, single-blind trial in two University Hospital Intensive Care Units in Spain. METHODS: We enrolled 50 patients with diabetes mellitus or stress hyperglycemia with basal glycemia > or =160 mg/dl and indication for enteral nutrition > or =5 days. Patients with severe kidney failure, liver failure or obesity were excluded from the study. In the first 48 h of admission, after randomization, 26 patients received the study diet and 24 patients received the control diet. The variables were monitored for 14 days. The Harris-Benedict formula with a fixed stress factor of 1.2 was used to calculate caloric needs. Insulin was administered by continuous infusion. An intention-to-treat analysis was performed. RESULTS: On admission, there were no differences between the study and control group in plasma glucose levels (mg/dl) (190.9+/-45 vs 210.3+/-63) and capillary glucose levels (mg/dl) (226.1+/-73 vs 213.8+/-67). After the feeding trial, there were differences between the study and control group in plasma glucose levels (mg/dl) (176.8+/-44 vs 222.8+/-47, P=0.001), capillary glucose levels (mg/dl) (163.1+/-45 vs 216.4+/-56, P=0.001), insulin requirements/day (IU) 8.73 (2.3-27.5) vs 30.2 (21.5-57.1) (P=0.001), insulin/received carbohydrates (UI/g) 0.07 (0.02-0.22) vs 0.18 (0.11-0.35) (P=0.02) and insulin/received carbohydrates/kg 0.98 (0.26-3.59) vs 2.13 (1.44-4.58) (P=0.04). These differences remain in a day-to-day comparison. There were no differences in the analytical tests, or in digestive or infectious complications. Intensive Care Unit length of stay, mechanical ventilation and mortality were similar in both groups. CONCLUSIONS: Hyperglycemic critically ill patients fed with a high-protein diet with a similar caloric percentage of fat and carbohydrates show a significant reduction in plasma glucose levels, capillary glucose levels and insulin requirements in comparison to patients on a conventional high-protein diet. This better glycemic control do not modify Intensive Care Unit length of stay, infectious complications, mechanical ventilation and mortality.

APACHE↗