ABSTRACT
SUMMARY: In neural regulation of the endocrine pancreas, there is much evidence to suggest that vagal efferents alter insulin and glucagon secretion, but less information on the effects of vagal afferents. In this study, we investigated the role and function of afferent fibers of the vagus nerve in normal and ventromedial hypothalamic (VMH) lesioned rats with marked hyperinsulinemia. In normal rats, hepatic vagotomy was associated with intraperitoneal (ip) arginine-induced enhancement of insulin and glucagon secretion without an accompanying change in blood glucose levels, ip leucine induced enhancement of insulin secretion accompanied by a decrease in blood glucose levels, and ip alanine-induced enhancement of glucagon secretion accompanied by an increase in blood glucose levels. In VMH lesioned rats with marked hyperinsulinemia, none of these amino acids caused significant changes in insulin and glucagon secretion. We conclude that amino acid sensors in normal rats inhibit excess release of pancreatic hormones induced directly by intake of amino acids, such as that in excess protein ingestion, and maintain blood glucose levels within the normal range. In contrast, in VMH lesioned rats with marked hyperinsulinemia, the function of the amino acid sensors is masked due to the marked hyperinsulinemia in these rats.:
ABSTRACT
UNLABELLED: Aims/Introduction: The effects of 5-day voluntary exercise on muscle damage and muscle protein degradation were investigated in a streptozotocin-induced rat model of moderately glycemic, uncontrolled, type 2 diabetes. MATERIALS AND METHODS: In the preliminary experiment, an oral glucose tolerance (1.0 g/kg) test was carried out to confirm the development of diabetes 3 days after streptozotocin treatment (30 mg/kg). In the genuine experiment, rats were divided into four groups: (i) non-diabetic rats without exercise (controls); (ii) non-diabetic rats with exercise; (iii) diabetic rats without exercise; and (iv) diabetic rats with exercise. After 5 days of voluntary wheel running exercise, blood and 24-h urine were collected, and levels of serum creatine kinase, a marker of muscle damage, and 24-h urinary excretion of muscle degradation products were determined. RESULTS: Type 2 diabetic rats with insulin deficiency that exercised had higher serum creatine kinase and greater urinary excretions of creatinine, urea nitrogen and 3-methylhistidine compared with both type 2 diabetic rats with insulin deficiency and non-diabetic rats that did not exercise. However, there were no differences in serum creatine kinase and urinary excretions of creatinine, urea nitrogen and 3-methylhistidine between non-diabetic rats that did and did not exercise. CONCLUSIONS: These findings suggest that muscle damage is induced and muscle protein degradation are enhanced by chronic moderate exercise in moderately glycemic uncontrolled type 2 diabetic rats with insulin deficiency at an intensity level of exercise that does not affect muscle damage and muscle protein degradation in non-diabetic rats. (J Diabetes Invest, doi: 10.1111/j.2040-1124.2011.00130.x, 2011).
