Results of randomised controlled trials of tight glycaemic control in hospital inpatients might vary with population and disease state. Individualised therapy for different hospital inpatient populations and identification of patients at risk of hyperglycaemia might be needed. One risk factor that has received much attention is the presence of pre-existing diabetes. So-called stress hyperglycaemia is usually defined as hyperglycaemia resolving spontaneously after dissipation of acute illness. The term generally refers to patients without known diabetes, although patients with diabetes might also develop stress hyperglycaemia—a fact overlooked in many studies comparing hospital inpatients with or without diabetes. Investigators of several studies have suggested that patients with stress hyperglycaemia are at higher risk of adverse consequences than are those with pre-existing diabetes. We describe classification of stress hyperglycaemia, mechanisms of harm, and management strategies.

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While the benefits of tight glycemic control have not been definitive, there are patients who will receive insulin infusion therapy, and the suggestions in this article provide the structure for safe and effective use of this therapy.

. S.A. is a member of the scientific advisory panel for and has received honoraria and/or consulting fees from Takeda/Lilly.Abbreviations: ALT, alanine aminotransferase; AST, aspartate aminotransferase; FPG, fasting plasma glucose; LOCF, last-observation-carried-forward; ULN, upper limitof normal.A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances. Pioglitazone Hydrochloride Monotherapy Improves Glycemic Control in the Treatment of Patients With Type 2 DiabetesA 6-month randomized placebo-controlled dose-response studyOBJECTIVE -To evaluate the efficacy and safety of four doses of pioglitazone monotherapy in the treatment of patients with type 2 diabetes.RESEARCH DESIGN AND METHODS -There were 408 patients randomized in this multicenter double-blind placebo-controlled clinical trial. Patients who had HbA 1c Ն7.0%, fasting plasma glucose (FPG) Ն140 mg/dl, and C-peptide Ͼ1 ng/ml were randomized to receive placebo or 7.5, 15, 30, or 45 mg pioglitazone administered once a day for 26 weeks.RESULTS -Patients treated with 15, 30, or 45 mg pioglitazone had significant mean decreases in HbA 1c (range Ϫ1.00 to Ϫ1.60% difference from placebo) and FPG (Ϫ39.1 to Ϫ65.3 mg/dl difference from placebo). The decreases in FPG were observed as early as the second week of therapy; maximal decreases occurred after 10-14 weeks and were maintained until the end of therapy (week 26). In the 15-, 30-, or 45-mg pioglitazone groups, there were significant mean percent decreases in triglycerides, significant mean percent increases in HDL cholesterol, and only small percent changes in total cholesterol and LDL. The subset of patients naive to therapy had greater improvements in HbA 1c and FPG (difference from placebo of Ϫ2.55% and Ϫ79.9 mg/dl for the 45-mg group) compared with previously treated patients. The overall adverse event profile of pioglitazone was similar to that of placebo. There was no evidence of drug-induced hepatotoxicity or drug-induced elevations of alanine aminotransferase levels in this study.CONCLUSIONS -Pioglitazone monotherapy significantly improves HbA 1c and FPG while producing beneficial effects on serum lipids in patients with type 2 diabetes with no evidence of drug-induced hepatotoxicity.

Objective The objective is to formulate clinical practice guidelines for the treatment of diabetes in older adults. Conclusions Diabetes, particularly type 2, is becoming more prevalent in the general population, especially in individuals over the age of 65 years. The underlying pathophysiology of the disease in these patients is exacerbated by the direct effects of aging on metabolic regulation. Similarly, aging effects interact with diabetes to accelerate the progression of many common diabetes complications. Each section in this guideline covers all aspects of the etiology and available evidence, primarily from controlled trials, on therapeutic options and outcomes in this population. The goal is to give guidance to practicing health care providers that will benefit patients with diabetes (both type 1 and type 2), paying particular attention to avoiding unnecessary and/or harmful adverse effects.

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As obesity is a major risk factor for noninsulin-dependent diabetes mellitus, adipose tissue may generate a mediator that influences the activity of insulin on various target tissues. Recent evidence suggests that a cytokine, tumor necrosis factor-alpha (TNF alpha), may serve this role. This study investigates whether the expression of TNF alpha and its receptors is modulated during drug treatment to reduce insulin resistance. The effects of moderate weight loss by dietary restriction were also examined. We show here that a marked induction of TNF alpha mRNA occurs in adipose tissues from a mouse model of obesity-linked diabetes (KKAy) compared to that in nondiabetic mice (C57). Likewise, RNA transcripts encoding TNF R2 receptors (p75) were significantly increased in fat tissues of the obese diabetic animals. In muscle from these diabetic animals, RNA transcripts encoding both TNF R1 (p55) and R2 were significantly elevated, although R2 transcript abundance was less elevated than in fat. We also observed that the overexpression of mRNA for TNF alpha and both of its receptors could be at least partly normalized by treatment of the diabetic animals with the insulin-sensitizing agent pioglitazone. Treating of the obese diabetic animals by food restriction reduced the expression of mRNA for TNF R2 in muscle, but not fat. These results clearly indicate that gene expression for the TNF systems can be regulated by an insulin-sensitizing drug and reduction of body weight. Such findings support a role for this cytokine in the insulin-resistant diabetic state and show its modulation by therapies that reverse the disorder.