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A number of circuits controlling feed intake have been identified in rodents in whichcirculating dietary metabolites are detected by the brainstem and the hypothalamusconverting these input signals to anorexic responses. Dietary metabolites used by dairycows, however, are not identical with those of rodents calling for the elucidation of feedingrelatedpathways in ruminants. In the present study we examined potentially relevant plasmametabolites and hypothalamic signalling pathways in <i>ad libitum</i> and restrictively fed earlylactating dairy cows. 60 h feed energy restriction led to significantly increased non-esterifiedfatty acid (NEFA), Gln, Gly, His, and 3-Me-histine but decreased Asp, Asn, beta-Ala, Tyr, andTrp concentrations. In immunohistochemical studies, we found that feed energy restriction isassociated with elevated numbers of parvocellular but not magnocellular orexin A neurons inthe lateral, dorsomedial and posterior hypothalamic area. In parvocellular orexin A neuronswe determined complete colocalisation with cFOS in energy restricted cows. In the majority oforexin A neurons we further found colocalisation with activated adenosine monophosphateactivated kinase (AMPK) as well as with peroxisome proliferator-activated receptor-gamma(PPARγ). Feed restriction also induced activation (phosphorylation) of AMPK and increasedexpression of PPARγ when Western Blots were normalized to β-actin. These results suggestthat orexin A associated with AMPK and PPARγ signalling is involved in the control of energyhomeostasis of dairy cows

Hypothalamic orexin A expression and the involvement of AMPK and PPAR-gamma signalling in energy restricted dairy cows