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Background Diabetes in pregnancy may result in unfavourable maternal and neonatal outcomes. Exercise was proposed as an additional strategy to improve glycaemic control. The effect of exercise during pregnancies complicated by diabetes needs to be assessed. Objectives To evaluate the effect of exercise programs, alone or in conjunction with other therapies, compared to no specific program or to other therapies, in pregnant women with diabetes on perinatal and maternal morbidity and on the frequency of prescription of insulin to control glycaemia. To compare the effectiveness of different types of exercise programs on perinatal and maternal morbidity. Search methods We searched the Cochrane Pregnancy and Childbirth Group's Trials Register (31 December 2005). We updated this search on 1 October 2009 and added the results to the awaiting classification section. Selection criteria All known randomised controlled trials evaluating the effect of exercise in diabetic pregnant women on perinatal outcome and maternal morbidity. Data collection and analysis We evaluated relevant studies for meeting the inclusion criteria and methodological quality. Three review authors abstracted the data. For all data analyses, we entered data based on the principle of intention to treat. We calculated relative risks and 95% confidence intervals for dichotomous data. Main results Four trials, involving 114 pregnant women with gestational diabetes, were included in the review. None included pregnant women with type 1 or type 2 diabetes. Women were recruited during the third trimester and the intervention was performed for about six weeks. The programs generally consisted in exercising three times a week for 20 to 45 minutes. We found no significant difference between exercise and the other regimen in all the outcomes evaluated. Authors' conclusions There is insufficient evidence to recommend, or advise against, diabetic pregnant women to enrol in exercise programs. Further trials, with larger sample size, involving women with gestational diabetes, and possibly type 1 and 2 diabetes, are needed to evaluate this intervention. [Note: The six citations in the awaiting classification section of the review may alter the conclusions of the review once assessed.]

Basal and postprandial somatostatin-like immunoreactivity (SLI) is elevated in the peripheral venous plasma of chronic alloxan-diabetic dogs. To determine if this hypersomatostatinemia was the consequence of increased somatostatin release from the pancreas, stomach, or both, plasma SLI was measured in the pancreaticoduodenal, antral, and fundic veins and in the inferior vena cava in response to stimulation by a gastric liver test meal, followed by an intragastric HCl load. Basal and postprandial inferior vena caval plasma SLI levels were significantly higher than the control level (P less than 0.05-0.001), confirming earlier findings. Basal pancreatic venous SLI was 780 +/- 45 pg/ml in the diabetic dogs and 493 +/- 65 pg/ml in the controls (P less than 0.02). In response to the liver meal at pH 7, the incremental pancreatic venous SLI level in the diabetic dogs was 1630 +/- 95 pg/ml, and after HCl it rose to 9479 +/- 384 pg/ml compared to 938 +/- 80 and 4677 +/- 192 pg/ml, respectively, in the controls (P less than 0.02 and P less than 0.005). However, antral and fundic venous SLI levels in the diabetic dogs did not differ from the controls in either basal or stimulated states. The present data demonstrate that the pancreas and not the stomach is the probable source of the peripheral hypersomatostatinemia of alloxan-diabetic dogs.

Recent studies have demonstrated that an acidified liver meal stimulates insulin release and raises plasma glucose levels. To examine the mechanism of these changes, a liver extract test meal at either pH7 or at pH2 was instilled into the stomach of dogs with a bisected pylorus and a gastric fistula during the infusion of either cimetidine, a specific H2-receptor antagonist, or a saline control. In response to the meal at pH2 insulin, glucagon and glucose levels rose significantly and were not significantly changed by the infusion of cimetidine. In response to the liver meal at pH7 a late rise in plasma glucagon levels was observed while plasma insulin and glucose did not change significantly; however, during the infusion of cimetidine a significant rise in plasma insulin and glucose levels occurred. The present data suggest that H2-receptors participate in an inhibitory mechanism with respect to the insulin and glucose response during the gastric phase of a neutral meal, but they do not seem to be involved in the rise in insulin and glucose observed in response to an acidified gastric meal.