Search

Exercise, along with dietary intervention, represents first-line therapy for diabetes mellitus. Aerobic exercise is recommended for its beneficial effects on glucose control as well as its abilities to retard the progression of other comorbidities common in patients with diabetes, such as cardiovascular disease. The capability of aerobic exercise to improve glycemic control in diabetes is well documented, although adherence to exercise regimens is problematic. More recently, the glucose- lowering effects of resistance training have also been documented; this form of exercise has additional benefits, such as the capability to counteract sarcopenia, which is common in older people with type 2 diabetes. Exercise in people with diabetes, however, also can present significant challenges to glycemic control. Excessive glucose lowering can occur under certain conditions, enhancing the threat of hypoglycemia; in other situations, hyperglycemia can be accentuated. An understanding of the interactions between specific antidiabetic medications and various forms and intensities of exercise is essential to optimizing glycemic control while minimizing the potential for acute derangements in plasma glucose levels. Exogenous forms of insulin and agents that stimulate insulin secretion in a glucose-independent manner (such as sulfonylureas and glinides) increase the propensity for hypoglycemia during low- to moderate-intensity aerobic exercise. In contrast, exercise protocols characterized by high intensity are more likely to result in episodes of hyperglycemia. Strategies to minimize inappropriate swings in glycemic control are reviewed. [ABSTRACT FROM AUTHOR]

We evaluated the effects of two thiazolidinediones (TZDs), the potent PPARγ agonist rosiglitazone currently being used to treat diabetes, and a structurally similar experimental compound that is a poor PPARγ agonist, in a non-diabetic, established hypertension model with continuous measurement of blood pressure by telemetry. Hypertension was induced in male Dahl salt-sensitive rats by a three-week pre-treatment with 4% salt before initiation of treatment. Fasting blood samples were taken for analysis of a biomarker panel to assess metabolic, anti-inflammatory and antioxidant activity of the treatments. Both TZDs significantly reduced both systolic and diastolic blood pressure. When used at the maximally effective doses established for metabolic improvement, both compounds produced equivalent reduction in lipids and elevation of adiponectin, yet the poorer PPARγ agonist produced significantly greater reductions in blood pressure. Neither compound had a significant effect on circulating glucose or insulin in this animal model.The data demonstrate that these TZDs lower blood pressure significantly in Dahl rats and that this cardiovascular pharmacology is not directly correlated with the metabolic actions or with the magnitude of PPARγ activation. These data suggest that it may be possible to find insulin-sensitising agents that have beneficial cardiovascular pharmacology with broad applications for disease prevention. [ABSTRACT FROM PUBLISHER]

Presents information on a study regarding the therapeutic effect of lithium on glucose transport in rat adipocytes. Methodology; Glucose transport studies; Statistical analysis; Experimental results.

Discusses the regulation of glutamine:fructose-6-phosphate aminotransferase (GFA) by cAMP-dependent protein kinase. Rate-limiting enzyme in hexosamine biosynthesis; Potential sites for phosphorylation; Effects of phosphatase inhibitors on GFA activity in vitro; Effects of PKA treatment on purified GFA; Effect of forskolin on GFA enzyme.

It has been hypothesized that increased production of tumor necrosis factor-alpha (TNF-alpha) plays a role in causing the insulin resistance associated with obesity. Obesity with insulin resistance is associated with increased production of TNF-alpha by fat cells. Exposure of 3T3-L1 adipocytes to TNF-alpha for 3-4 days makes them insulin resistant. TNF-alpha has also been reported to rapidly (15-60 min) cause insulin resistance, with a decrease in insulin-stimulated tyrosine phosphorylation, in a number of cultured cell lines. Because skeletal muscle is the major tissue responsible for insulin-stimulated glucose disposal, we performed the present study to determine if acute exposure to TNF-alpha causes insulin resistance in muscle. We found that exposure of soleus muscles to 6 nmol/l TNF-alpha for 45 min in vitro had no inhibitory effect on insulin-stimulated tyrosine phosphorylation of the insulin receptor or insulin receptor substrate 1 (IRS-1) or on phosphatidylinositol 3-kinase association with IRS-1. Incubation of epitrochlearis and soleus muscles with 6 nmol/l TNF-alpha for 45 min or 4 h had no effect on insulin-stimulated 2-deoxyglucose (2-DG) uptake. Treatment of epitrochlearis muscles with 2 nmol/l TNF-alpha for 8 h also had no effect on insulin-stimulated 2-DG uptake. We conclude that in contrast to Fao hepatoma cells and 3T3-L1 fibroblasts, skeletal muscle does not become insulin resistant in response to short-term exposure to TNF-alpha. [ABSTRACT FROM AUTHOR]