Different effects of whole milk and a fermented milk with the same fat and lactose content on gastric emptying and postprandial lipaemia, but not on glycaemic response and appetite.

Longitudinal studies indicate that milk and fermented milk products lower basal plasma cholesterol concentrations, despite their high content of saturated fat, and therefore have favourable health effects. However, there have been few studies on the postprandial effects of milk products. The present study compared the effect of whole milk with a fermented milk, A-38, on postprandial carbohydrate and lipid metabolism, gastric emptying and appetite. Eight healthy young men participated. On the two test days, they arrived fasting for collection of baseline values before consuming the meals, which for a 75 kg subject consisted of 1.4 litre milk or fermented milk, plus 165 mg [13C]acetate (for later determination of gastric emptying by a [13C]acetate breath test). Lactose (15 g) was added to the A-38 meal to equalize the lactose content. Postprandially the A-38 meal resulted in a slower gastric emptying rate than milk (P<0.001). Furthermore, the A-38 meal resulted in a greater increase and a quicker decrease of the triacylglycerol content in all lipoprotein fractions (LDL-fraction, P<0.05; other fractions, P<0.001) and of the gastrointestinal hormones (cholecystokinin and peptide YY, P<0.05; gastric inhibitory polypeptide and glucagon-like polypeptide-1, P<0.001). There were no significant differences in appetite sensations (measured by visual analogue scale) or in the glucose and insulin response (P>0.10). The slower emptying rate of the liquid phase after the A-38 meal is probably due to the higher viscosity of A-38. The lower and more prolonged triacylglycerol response after the milk meal might be caused by coagulation of milk in the stomach.

Serotonin inhibits glutamate- but not PACAP-induced per gene expression in the rat suprachiasmatic nucleus at night.

Circadian rhythms of physiology and behaviour generated by the brain's biological clock located in the suprachiasmatic nucleus are entrained by light via the retinohypothalamic tract. Two neurotransmitters, glutamate and pituitary adenylate cyclase-activating polypeptide (PACAP), found in this monosynaptic pathway mediate the effects of light to the clock. It is well known that not only light entrains the clock. Nonphotic cues mediated by neurotransmitters such as serotonin reaching the suprachiasmatic nucleus from the midbrain raphe nucleus modulate light-induced phase shifts at night. Two clock genes, per1 and per2, have been attributed a role in light-induced phase shift. In the present study, using an in vitro brain slice model and quantitative in situ hybridization for per1 and per2, we have shown that serotonin induces per1 gene expression at late subjective night but not at early night. Furthermore, serotonin application before glutamate or PACAP blocked glutamate-induced per1 expression at early night and per2 gene expression at late night. In contrast, serotonin did not influence PACAP-induced per gene expression at late night. Triple antigen immunohistochemistry and confocal microscopy supported both a pre- and post-synaptic interaction of retinohypothalamic tract (PACAP-immunoreactive) and serotonin projections on vasoactive intestinal peptide- and gastrin-releasing peptide-containing cell bodies in the ventro-lateral suprachiasmatic nucleus. Our findings suggest that the per genes could be the molecular target for the modulatory effects of serotonin on light signalling to the clock.