| dc.description.abstract |
Recent studies have established a fimctional correlation of serotonergic and
adrenergic function in the brain regions with insulin secretion in diabetic rats (Vahabzadeh
et al., 1995). Administration of 5-HT”. agonist 8-OH-DPAT to conscious rats caused an
increase in blood glucose level. This increase in blood glucose is due to inhibition of
insulin secretion by increased circulating EPI (Chaouloff et al., 1990a; Chaouloff et al.,
1990d; Chaoulo1T& Jeanrenaud, 1987). The increase in EPI is brought about by increased
sympathetic stimulation. This increase can lead to increased sympatho-medullary
stimulation thereby inhibiting insulin release (Bauhelal & Mir, 1993, Bauhelal & Mir,
1990a; Chaouloffet al., 1990d). Also, studies have shown that Gi protein in the liver has
been decreased in diabetes which will increase gluconeogenesis and glycogenolysis
thereby causing hyperglycaemia (Pennington, 1987). Serotonergic control is suggested to
exert different effects on insulin secretion according to the activation of different receptor
subclasses (Pontiroli et al., 1975). In addition to this mechanism, the secretion of insulin
is dependent on the turnover ratio of endogenous 5-hydroxy tryptophan (5-HTP) to 5-HT
in the pancreatic islets (Jance er al., 1980). The reports so far stated does not explain the complete mechanism and the subclass of 5-HT receptors whose expression regulate insulin secretion in a diabetic state. Also, there is no report of a direct regulation of insulin secretion by 5-HT from the pancreatic islets even though there are reports stating that the pancreatic islets is a rich source of 5-HT (Bird et al., 1980). Therefore, in the present study the mechanism by which 5-HT and its receptors regulate insulin secretion from pancreatic [3-cells was investigated. Our results led to the following hypotheses by which 5-HT and its receptors regulate the insulin secretion. |
en_US |