[The central nervous system-endocrine pancreas axis].

Area of Science:

• Neuroendocrinology
• Metabolic Regulation
• Physiology

Background:

• Evidence suggests glucose- and insulin-sensitive sites exist in the central nervous system (CNS).
• Activation of these sites influences the parasympathetic nervous system, impacting peripheral insulin secretion and glucose homeostasis.
• Disruptions in CNS energy substrates can lead to increased peripheral glycemia.

Purpose of the Study:

• To explore the role of the central nervous system in regulating glucose and insulin.
• To investigate the link between hypothalamic factors, parasympathetic activity, and insulin secretion.
• To understand the mechanisms underlying hyperinsulinemia and obesity in genetically predisposed rats.

Main Methods:

• Review of existing results on CNS regulation of glucose and insulin.
• Analysis of effects of ventromedial hypothalamus (VMH) lesions and vagotomy on insulin secretion.
• Examination of insulin response to glucose load in genetically pre-obese rats (fa/fa) and the effect of atropine.
• Investigation of hypothalamic factors' activity on insulin secretion in vivo and in vitro.

Main Results:

• VMH lesions induce early hyperinsulinemia, abolished by vagotomy.
• Genetically pre-obese rats exhibit hyperinsulinemia in response to glucose, which is mitigated by atropine, suggesting parasympathetic involvement.
• Cephalic phase insulin secretion appears to optimize post-meal insulin response and glucose tolerance.
• Hypothalamic factors demonstrate insulin secretion-promoting activity.

Conclusions:

• The CNS plays a crucial role in modulating peripheral glucose and insulin levels via the parasympathetic nervous system.
• Hyperinsulinemia and subsequent obesity may be linked to parasympathetic overactivity and impaired CNS energy sensing.
• Further research is needed to clarify the nature (humoral vs. neural) of hypothalamic factors influencing insulin secretion.