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In healthy persons, glucose homeostasis maintains blood glucose levels between 70 and 130 mg/dl despite perturbations by meals, fasting, and exercise. Long-term follow-up of diabetic patients has suggested that "good control" of blood sugar levels minimizes the long-term complications of diabetes, such as retinopathy, nephropathy, and atherosclerosis. It now seems likely the products of insulin-independent metabolic pathways in epithelial and endothelial cells leading to polyol formation and protein glycosylation may be factors in the genesis of retinopathy, neuropathy, nephropathy, and premature atherosclerosis of diabetic patients. Dietary complex carbohydrates of various type, including those rich in dietary fiber, which are the cell walls of fruits, vegetables, and cereals, may slow the rate of absorption of glucose from those diets and contribute to a lowering of the postprandial glucose peak. Glycemic responses to various foods compared to glucose have been studied and show a large variation, which is dependent upon gastric emptying, overall effects on rate of hydrolysis and absorption of glucose from food mixtures. Dietary sucrose seems to cause a degree of insulin resistance. The active part of the disaccharide is fructose, which does not elicit an acute insulin response, but appears indirectly to increase insulin levels in both animals and man. Sucrose in animals appears to promote obesity more than glucose because of its lack of stimulation of thermogenesis. Xylitol has been used as a sweetener and as a sugar substitute in total parenteral nutrition. It is a paradox that the most physiological of sugars (glucose) can be a menace at high concentrations. The use of nonphysiological sugars or their derivatives in diabetics and patients with special needs, such as TPN, requires much more investigation to develop a sound rationale in nutrition management.

SUMMARYIn an attempt to confirm the reported high incidence of raised serum gastrin levels in patients with rheumatoid arthritis (RA), gastrin concentrations were estimated in 54 patients. Only three patients (6%) had basal hypergastrinaemia. The heptadecapeptide (G17) and total carboxylterminal immunoreactive gastrin responses to a standard protein meal were measured by specific radioimmunoassay in these three patients and in nine normogastrinaemic RA patients displaying the same age range. The three hypergastrinaemic patients showed significantly greater and more prolonged G17 and total carboxylterminal immunoreactive gastrin responses to the meal compared with the normogastrinaemic RA patients (p < 0 02). Two of these three patients agreed to have an acid output study (pentagastrin 6 ,tg/kg subcutaneously) and gastric mucosal biopsies taken for histology. Both were found to be achlorhydric and to have atrophic gastritis. This study suggests that basal hypergastrinaemia in RA patients is considerably less common than previously reported and, when present, is associated with achlorhydria. In addition, the incidence of achlorhydria in rheumatoid arthritis is similar to that found in a normal age-matched population.

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