BackgroundPhysical exercise improves glucose metabolism and insulin sensitivity. Brain-derived neurotrophic factor (BDNF) enhances insulin activity in diabetic rodents. Because physical exercise modifies BDNF production, this study aimed to investigate the effects of chronic exercise on plasma BDNF levels and the possible effects on insulin tolerance modification in healthy rats.MethodsWistar rats were divided into five groups: control (sedentary, C); moderate- intensity training (MIT); MIT plus K252A TrkB blocker (MITK); high-intensity training (HIT); and HIT plus K252a (HITK). Training comprised 8 weeks of treadmill running. Plasma BDNF levels (ELISA assay), glucose tolerance, insulin tolerance, and immunohistochemistry for insulin and the pancreatic islet area were evaluated in all groups. In addition, Bdnf mRNA expression in the skeletal muscle was measured.Principal FindingsChronic treadmill exercise significantly increased plasma BDNF levels and insulin tolerance, and both effects were attenuated by TrkB blocking. In the MIT and HIT groups, a significant TrkB-dependent pancreatic islet enlargement was observed. MIT rats exhibited increased liver glycogen levels following insulin administration in a TrkB-independent manner.Conclusions/SignificanceChronic physical exercise exerted remarkable effects on insulin regulation by inducing significant increases in the pancreatic islet size and insulin sensitivity in a TrkB-dependent manner. A threshold for the induction of BNDF in response to physical exercise exists in certain muscle groups. To the best of our knowledge, these are the first results to reveal a role for TrkB in the chronic exercise-mediated insulin regulation in healthy rats.

These results indicate that high-intensity chronic exercise reduces BDNF protein level in fast muscles and increases Bdnf mRNA levels in slow muscles.

Arginine-vasopressin mediates central and peripheral glucose regulation in response to carotid body receptor stimulation with Na-cyanide. J Appl Physiol 100: 1902-1909, 2006. First published February 23, 2006 doi:10.1152/japplphysiol.01414.2005.-Hypoxic stimulation of the carotid body receptors (CBR) results in a rapid hyperglycemia with an increase in brain glucose retention. Previous work indicates that neurohypophysectomy inhibits this hyperglycemic response. Here, we show that systemic arginine vasopressin (AVP) induced a transient, but significant, increase in blood glucose levels and increased brain glucose retention, a response similar to that observed after CBR stimulation. Comparable results were obtained after intracerebral infusion of AVP. Systemic AVP-induced changes were maintained in hypophysectomized rats but were not observed after adrenalectomy. Glycemic changes after CBR stimulation were inhibited by pharmacological blockage of AVP V1a receptors with a V1a ]-vasopressin). Importantly, local application of micro-doses of this antagonist to the liver was sufficient to abolish the hyperglycemic response after CBR stimulation. These results suggest that AVP is a mediator of the hyperglycemic reflex and cerebral glucose retention following CBR stimulation. We propose that hepatic activation of AVP V1a receptors is essential for this hyperglycemic response.chemoreceptors; central nervous system respiration RECENT WORK SUGGESTS that the carotid body receptors (CBR), in addition to their classical role sensing O 2 , CO 2 , and pH levels (19,43), also function as receptors of glucose concentration entering the cephalic circulation (1,5,30,41,42). Changes in blood glucose concentration in the carotid sinusbody influence the amount of glucose retained by the brain (6), and the injection of sodium cyanide (NaCN) into the local circulation of the carotid sinus induces a rapid hyperglycemic reflex with a rise in brain glucose retention (1). Unloading of carotid baroreceptors also induces rapid glucose adjustments to regulate plasma osmolality during hemorrhage (28). Experimentally induced low-glucose levels increase catecholamine secretion from carotid body glomus cells in a concentrationdependent manner (41), indicating that this structure is very sensitive to glucose concentration.The efferent pathway for the glycemic reflexes initiated in the carotid sinus region is not fully understood. Previous experiments indicate the participation of the neurohypophysis and adrenal glands, suggesting that the effects of these two glands on CBR hyperglycemic reflexes are humoral (2). A reflex discharge of neurohypophyseal secretion occurs after centripetal stimulation of the vagus nerve (23), and it is known that peripheral receptors connected to the vagus nerve (aortic baro-and chemoreceptors) or associated with the glossopharyngeal nerve (carotid baro-and chemoreceptors) mediate some of their effects through the pituitary (44). It is not known, however, what factors secreted by neurohypophysis are required to elicit...

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