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Glucose normalization

Glucose normalization

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Published in Volume 87, Issue 2 on February 1, J Clin Invest. Published February 1, - Version history. Abstract Evidence is emerging for a direct role of glucose, independent of changes in insulin, in the regulation of cellular glucose transport and glucose utilization in vivo.

View PDF of the complete article page page Over the intervening years since subsequent studies have provided conflicting evidence of benefit, and intensive insulin therapy has become an increasingly controversial treatment.

The long awaited results of the largest ever randomized controlled trial of intensive insulin therapy, known as the NICE-SUGAR study, were recently published. Results suggest, in stark contrast to those of the Belgium study, that patients gain no benefit from normalization of blood glucose by intensive insulin therapy.

For the NICE-SUGAR study critically ill patients admitted to intensive care units of all types in Australia, New Zealand, Canada and United Sates were randomly assigned within 24 hours of admission to one of two treatment groups. The aim for the first group was to maintain blood glucose within normal limits 4.

Those in the second conventionally treated group were only given insulin if blood glucose exceeded Primary end point was death from any cause within 90 days of admission. Of the patients assigned to intensive insulin therapy, There was no difference between the groups for several measures of morbidity length of stay in intensive care, length of time on mechanical ventilation, etc.

NICE-SUGAR study investigators conclude that normalizing blood glucose concentration "does not necessarily benefit patients and may be harmful". In an accompanying editorial the authors discuss the implication of the provocative results of this important study for routine care of the critically ill.

May contain information that is not supported by performance and intended use claims of Radiometer's products. We performed hyperinsulinemic-euglycemic clamps with indirect calorimetry and vastus lateralis muscle biopsies in eight type 2 diabetic patients who had poor glycemic control HbA 1c Improved glycemic control increased insulin-stimulated glucose disposal 5.

There was no improvement in insulin-stimulated glucose oxidation 3. All of the increase in insulin-stimulated glucose disposal could be accounted for by increased glycogen synthesis, which is likely attributable to increased activation of glycogen synthase by insulin.

Insulin resistance in skeletal muscle is a characteristic feature of type 2 diabetes 1. The insulin resistance is thought to derive from two components. One component is primary or hereditary in nature, and is present before the development of diabetes and its attendant metabolic abnormalities.

Abundant evidence shows that normal glucose-tolerant individuals with a strong family history of type 2 diabetes are insulin resistant 2 — 7 , thereby suggesting a hereditary component to the defect in insulin action. The second component of the muscle insulin resistance is acquired secondary to alterations in the metabolic milieu, including elevated plasma glucose 8 — 11 , free fatty acid FFA 12 — 14 , and insulin 15 — 17 levels.

Experimental hyperinsulinemia has been shown to cause insulin resistance both in vitro 10 , 18 and in vivo 15 — 17 , Similarly, a physiological elevation in plasma FFA concentrations has been shown to induce muscle insulin resistance 20 — 22 Finally, chronic hyperglycemia itself is known to impair insulin action 8 , 9 , and reversal of hyperglycemia in rats with phlorizin 23 — 25 improves insulin sensitivity.

In type 1 diabetic patients, intensive insulin therapy also has been shown to augment insulin action 26 — Some 30 — 36 , but not all 37 , studies have shown that insulin therapy can improve insulin resistance in type 2 diabetic patients as well. However, the improvement in insulin resistance is less uniformly observed in type 2 than in type 1 diabetic subjects and, when observed, is of lesser magnitude.

No previous study has examined the biochemical basis for the improvement in insulin resistance observed after improved glycemic control with insulin in type 1 or type 2 diabetic individuals. Results from several recent studies in rodents have suggested that increased hexosamine biosynthesis leads to skeletal muscle insulin resistance in vivo and in vitro 38 — In other studies, glucose-induced activation of protein kinase C isoforms has been shown to interfere with insulin receptor signaling and produce insulin resistance 41 — Kurowski et al.

In the present study, we used a mixed-split insulin treatment regimen to produce tight glucose control in type 2 diabetic subjects in an attempt to determine the biochemical mechanisms responsible for impaired insulin-stimulated glucose disposal in skeletal muscle. Hyperinsulinemic-euglycemic clamps with indirect calorimetry and vastus lateralis muscle biopsies were performed while diabetic subjects were in poor glycemic control and again after they had sustained 3 months of near-normoglycemia through insulin therapy.

Insulin-stimulated whole-body glucose uptake, glucose oxidation, and nonoxidative glucose disposal primarily representing glycogen synthesis were quantified and compared with insulin-stimulated hexokinase HK II activity and mRNA levels and glycogen synthase activity in muscle biopsies.

The results demonstrated that improved glycemic control enhances insulin-stimulated glucose disposal, nonoxidative glucose disposal glycogen synthesis , and glycogen synthase activity, without improving glucose oxidation, hexokinase enzymatic activity, or hexokinase mRNA expression.

Eight subjects with poorly controlled type 2 diabetes five men and three women, aged 51 ± 3 years, BMI In all subjects, the diagnosis of type 2 diabetes was established using American Diabetes Association criteria. None of the patients had previously taken metformin or a thiazolidinedione.

Other than having type 2 diabetes, all subjects were in good general health as determined by medical history, physical examination, routine blood tests, urinalysis, and electrocardiogram.

No subject was taking any medication known to adversely affect glucose metabolism. In all subjects, body weight was stable for at least 4 months before the study. No subject participated in exercise on a regular basis. Subjects were instructed to maintain their usual diet and not to engage in any vigorous exercise for at least 3 days before the study.

The purpose, nature, and potential risks of the study were explained to all subjects, and their written consent was obtained before their participation. The protocol was approved by the Institutional Review Board of the University of Texas Health Science Center at San Antonio, TX.

All patients received a hyperinsulinemic-euglycemic clamp study with biopsies of the vastus lateralis muscle before and after 12 weeks of tight glycemic control, which was achieved with a mixed-split insulin treatment regimen see below.

The hyperinsulinemic-euglycemic clamps were performed at the General Clinical Research Center of the University of Texas Health Science Center at San Antonio, TX, as previously described Studies began at h after a h overnight fast.

A hand vein was cannulated in retrograde fashion, and the hand was placed in a heated box 60°C for sampling of arterialized blood. After min of bed rest, a percutaneous muscle biopsy was obtained with a Bergstrom cannula from the vastus lateralis muscle under local anesthesia Muscle biopsy specimens 75— mg were immediately blotted free of blood, frozen, and stored in liquid nitrogen until used.

Blood was drawn every 5—10 min during the last 30 min of the isotopic equilibration period for measurement of tritiated glucose radioactivity and plasma glucose, insulin, and FFA concentrations.

Continuous indirect calorimetry was performed with a ventilated hood system DeltaTrac, Sensor Medics, Anaheim, CA during the last 40 min of the tracer equilibration and insulin clamp periods for the measurement of carbohydrate and lipid oxidation rates.

Plasma glucose was measured every 5 min throughout the study with a glucose oxidase analyzer Beckman Instruments, Fullerton, CA. At the end of the study, a second percutaneous muscle biopsy was obtained from the opposite vastus lateralis muscle and then the insulin infusion was stopped.

After completion of the hyperinsulinemic-euglycemic clamp, all subjects met with a diabetes nurse educator and were instructed in home blood glucose monitoring. Then patients stopped their oral hypoglycemic medication and were started on a multiple insulin injection regimen, which consisted of bedtime and morning NPH insulin with two injections of regular insulin 20—30 min before breakfast and dinner.

On average, the diabetic subjects took 32 ± 5 units of NPH insulin and 9 ± 1 units of regular insulin in the morning, 14 ± 2 units of regular insulin with dinner, and 24 ± 2 units of NPH insulin at bedtime. Home self-monitoring of blood glucose concentrations was performed four times per day.

Subjects spoke with the investigators two to three times per week and returned to the clinic every 2 weeks for a review of blood glucose self-monitoring and insulin dosage adjustment. HbA 1c was measured every month and twice during the last week of the study.

After 12 weeks of intensified glycemic control, the hyperinsulinemic-euglycemic clamp study with indirect calorimetry and muscle biopsies was repeated in all subjects, as described above.

Fat-free mass FFM was measured before and after intensified glycemic control by a bioelectrical impedance method RJL Systems, Clinton, MI. Glycogen synthase, HKI, and HKII activities were assayed as previously described, with some minor modifications Homogenates were centrifuged at 13, g , and the supernatant soluble fraction was removed and saved for assay of glycogen synthase activity.

Glycogen synthase activity was assayed in the soluble fraction using 0. Glycogen synthase fractional velocity GS fv was calculated as the ratio of the activity determined using 0.

Hexokinase mRNA content was determined in total RNA isolated from a portion of each muscle biopsy using an RNase protection assay Ambion, Austin, TX , as previously described Muscle was extracted using a guanidinium isothiocyanate method Tel-Test, Friendswood, TX.

The content of HKI and HKII mRNA was determined on 4-μg aliquots of total RNA. Riboprobes were generated that would yield protected products of nt for HKI and nt for HKII 48 , HKI and HKII RNAs were quantified using a PhosphorImager Molecular Dynamics, Sunnyvale, CA and were normalized to a 28S rRNA internal control signal Ambion, Austin, TX.

Thus, within each sample, 28S rRNA, HKI mRNA, and HKII mRNA were quantified simultaneously. All signals PhosphorImage density units were normalized to the 28S rRNA value within that sample.

Insulin stimulation of HK mRNA was then assessed by setting the basal value for each subject to 1. Therefore, values for HKI and HKII mRNA are expressed as dimensionless ratios. Plasma insulin concentration was determined by radioimmunoassay Diagnostic Product, Los Angeles, CA , and plasma FFA concentration was determined by an enzymatic method Wako Pure Chemical Industry, Osaka, Japan.

The rate of glucose oxidation was calculated from the rates of respiratory gas exchange, as previously described The rate of nonoxidative glucose disposal, which primarily represents muscle glycogen synthesis 54 , was calculated by subtracting the rate of glucose oxidation from the rate of total body glucose disposal during the hyperinsulinemic-euglycemic clamp.

Differences in glucose metabolic rates, enzyme activities, and mRNA levels before and after intensified glycemic control were compared for statistical significance by ANOVA or paired t test, where appropriate. Similarly, during the last 30 min of the hyperinsulinemic-euglycemic clamp, plasma FFA concentrations were more suppressed by insulin infusion after insulin therapy ± 30 vs.

When the diabetic subjects had poor glucose control, the basal rate of endogenous hepatic glucose production was 3. After 12 weeks of intensified insulin therapy, basal hepatic glucose production decreased to 3.

before insulin therapy , and the rate of glucose production during the insulin clamp was suppressed to 0. insulin clamp before insulin therapy. During the baseline insulin clamp study, glucose oxidation increased from 1.

After 12 weeks of insulin therapy, the increase in glucose oxidation during the insulin clamp from 1. Insulin-stimulated nonoxidative glucose metabolism, which primarily represents skeletal muscle glycogen synthesis, was significantly increased by insulin therapy from 0.

The increase in whole-body glucose disposal after 12 weeks of insulin therapy was primarily attributable to the increase in nonoxidative glucose disposal.

Douglas RogersNormalkzation RowoldGlucose normalization ChangMartha NormalizationnNormalizatiin R GoucoseJames GavinCharles KiloJoseph Glycose Williamson; Effect of Rapid Nlrmalization of Gludose Glucose Levels on Microvascular Dysfunction and Polyol Metabolism Glucose normalization Diabetic Rats. Diabetes 1 Glucose normalization ; 37 Skinfold measurement for obesity diagnosis : — Glucose normalization days after implantation of pumps, plasma insulin levels were twice normal levels and remained elevated 1. Plasma glucose levels and granulation tissue polyol levels were normalized within 2 days after initiation of insulin treatment. Plasma IGF-I levels were significantly increased 2 times by 2 days, but were not normalized until 7 days. In contrast, I-albumin permeation normalized at a much slower relatively linear rate and was still not completely normal after 14 days of insulin treatment. The relatively long lag time after normalization of plasma glucose and tissue polyol levels before near normalization of vascular permeability in this model isconsistent with corresponding observations on the relationship between improved glycemic control and normalization of microangiopathy and neuropathy in diabetic humans and animals.


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