Type 1 Diabetes: Effect Of Intensive Management

Although the autoimmune process may result in complete beta cell destruction, this is not always the case, particularly in the early stages of the disease in young adults. Before the development of serum c-peptide assays to assess insulin secretion in the presence of insulin therapy,

clinicians had noted that people with type 1 diabetes who were treated with insulin may have a “honeymoon period,” during which insulin requirements decrease, but metabolic control is maintained.
Subsequently, after the development of the c-peptide assay, it was apparent that this phenomenon was due to the fact that basal and stimulated insulin secretion can be maintained for years in some people with type 1 diabetes. The Diabetes Control and Complications Trial (DCCT) afforded a unique opportunity to study the natural history of type 1 diabetes longitudinally in a group 1441 of adolescents and adults with type 1 diabetes.

Furthermore, the design of the DCCT allowed analysis of the effect of standard vs. intensive glycaemic management on pancreatic c-peptide secretion, a good index of insulin secretion. Cross-sectional analyses of subjects screened for the trial demonstrated that a similar number of adults (45%) and adolescents (37%) with short diabetes duration (1-5 years) had evidence of insulin release with nutrient stimulation. The plasma levels of fasting and meal-stimulated c-peptide levels were closely correlated, and both declined with increasing duration of the disease. Among patients with diabetes for more than 5 years, 11 % of adults (18-39 years of age) compared with no adolescents (13-18 years of age) retained insulin secretory capacity. After one year of therapy, intensive glycemic treatment was associated with less of a decline in insulin secretory capacity than standard therapy.

Subsequently, the effect of intensive therapy on residual beta cell function was analyzed in 303 of the 855 DCCT patients with diabetes of 1-5 years’ duration who had c-peptide responses at baseline. Responders who had been receiving intensive therapy maintained a higher stimulated c-peptide level than responders receiving conventional therapy (57% risk reduction, p < 0.001). Maintenance of endogenous insulin secretion was associated with improved metabolic control, a lower risk of hypoglycemia, and a decreased rate of progression of retinopathy. The mechanism for the protective effect of intensive insulin therapy on islet function is not known. It may be due to a reduction of the glucotoxic effect of hyperglycemia on islet cell function or a slowing of the autoimmune process that leads to islet destruction. Whatever the mechanism, the results in the DCCT strongly support a strategy of intensive glycemic management with insulin from the time of first discovery of type 1 diabetes.

In a recently reported phase II trial in 35 patients with type 1 diabetes and residual beta cell function, plasma c-peptide concentrations after glucagon injection were maintained for 10 months in patients treated with an immunomodulatory material, heat shock protein. In the control group, c-peptide levels fell to a significantly greater degree than in the treated group. It was postulated that a shift from a proinflammatory t-helper-1 to an anti-inflammatory t-helper-2 population accounted for the results. Presumably, these promising studies will be followed with large-scale trials to determine whether this therapy can produce long-term maintenance of insulin secretion in type 1 diabetes.

Diabetes: New findings about food, weight, and exercise

Formerly, the diets prescribed for diabetics allowed very few carbohydrates but lots of proteins and fats. Then doctors discovered that such diets probably contributed in part to diabetics’ increased risks of heart disease and stroke.

Doctors now know that diets comprised of fiber and complex carbohydrates (fresh fruits instead of fruit juices, whole grains, legumes, pasta) can actually smooth out the body’s absorption of digested sugars into the bloodstream.

Dr. James Anderson of the University of Kentucky prescribes a diet in which about 50 percent of daily calories come from complex carbohydrates – starches. The diet is primarily fresh vegetables and fruits, plus dried beans, lentils, and peas.
Dr. Anderson says he can get the majority of Type I diabetics off insulin and can reduce the need for insulin by a third for Type II diabetics. “We have good evidence that the diets increase the sensitivity of the body to insulin,” he reports.

Essentially, the insulin molecule works by attaching itself to the molecules of the cell membrane, like a key fitting into a lock. The cell membrane is like a wall. The molecules attached to the “wall” are called receptors. They change in size and number. Studies at Yale University by Drs. Philip Felig and Ralph A. DeFronzo have found that the number of insulin receptors increases -and blood sugar levels drop – in diabetics who exercise regularly.

Doctors have always known that obesity increases the risk of developing Type II diabetes. Now they also know that overweight diabetics have fewer insulin receptors and that weight loss somehow reduces blood sugar levels by increasing the number of receptors.
Research into ways of stopping the death of the insulin-producing cells is going forward at a breathtaking pace. New treatments are constantly tested. The scientists are confident that they will find ways of controlling this killing disease.