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Effects of leptin on cat intestinal motility.

Laboratoire de Physiologie Neurovégétative, UMR CNRS 6153, UMR INRA, Faculté des Sciences et Techniques Saint-Jérôme, Université Aix-Marseille 3, Case postale 351-352, Avenue Escadrille Normandie Niemen, 13397 Marseille Cedex 20, France.

In a previous study, we established that leptin controls food intake and immune responses by acting on intestinal vagal chemosensitive mechanoreceptors via a functional link with interleukin-1 beta (Il-1 beta). Since the control of intestinal motility is one of the main roles of the vagal afferent fibres, we investigated the effects of leptin on intestinal electromyographic (EMG) activity which reflects intestinal motility. For this purpose, the effects of locally injected leptin on small intestine spontaneous EMG activity were studied in 23 anaesthetised cats. The EMG activity was recorded using bipolar electrodes implanted in the proximal small intestine. Leptin and Il-1 beta (0.1, 1 and 10 microg), administered through the artery irrigating the upper part of the intestine 20 min after cholecystokinin (CCK, 10 microg, I.A.), had significant (P < 0.001) excitatory effects on intestinal EMG activity. The effects of both substances were blocked by the endogenous interleukin-1 beta receptor antagonist (Il-1ra, 250 microg, I.A.), by atropine (250 microg, I.A.) and by vagotomy. In the absence of CCK, leptin and Il-1 beta had no effect on intestinal electrical activity. It can therefore be concluded that: (1) leptin is effective only after the previous intervention of CCK, (2) the enhancement of the electrical activity induced by leptin involves Il-1 beta receptors and the cholinergic excitatory pathway, (3) the modes whereby the leptin-induced enhancement of EMG activity occurs strongly suggest that these effects are due to a long-loop reflex involving intestinal vagal afferent fibres and the parasympathetic nervous system.

PMID: 12509494 [PubMed - indexed for MEDLINE]

Effects of interactions between interleukin-1 beta and leptin on cat intestinal vagal mechanoreceptors.

Laboratoire de Physiologie Neurovégétative (UMR CNRS 6153, UMR INRA 1147), Faculté des Sciences et Techniques Saint-Jérôme, Université Aix-Marseille 3, Cases postales 351-352, Avenue Escadrille Normandie Niemen, 13397 Marseille Cedex 20, France.

In a previous study, we established that leptin acts on chemosensitive intestinal vagal mechanoreceptors and that its excitatory effects are blocked by the endogenous interleukin-1beta receptor antagonist (Il-1ra). To determine how interleukin-1beta (Il-1beta) is involved in the action of leptin, we studied the effects of this drug on the single vagal afferent activities of intestinal mechanoreceptors in anaesthetized cats. For this purpose, the activity of 34 intestinal vagal mechanoreceptors was recorded via glass microelectrodes implanted in the nodose ganglion. Il-1beta (1 microg) administered into the artery irrigating the upper part of the intestine activated both the 16 leptin-activated units (type 1 units; P < 0.01) and the 12 leptin-inhibited units (type 2 units; P < 0.001), but had no effect on the six leptin-insensitive units. Cholecystokinin (CCK, 10 microg) induced an activatory response only in the two types of Il-1beta-sensitive units. When Il-1beta was administered after CCK, its excitatory effects on type 1 units were enhanced, whereas the excitatory effects on type 2 units were abolished. Pre-treatment with Il-1ra (250 microg) blocked all the effects of Il-1beta and the excitatory effects of leptin on type 1 units, whereas it enhanced the inhibitory effects of leptin on type 2 units. It can therefore be concluded that (i) leptin acts on intestinal vagal mechanoreceptors via Il-1beta in the case of the type 1 units and independently of Il-1beta in the case of the type 2 units, and (ii) type 1 and type 2 units belong to two different populations of vagal afferents that transmit different information about ingestion or inflammation to the CNS, depending on the chemical environment.

PMID: 14645453 [PubMed - indexed for MEDLINE]

PMCID: PMC1664812

三、1: J Feline Med Surg. 2002 Jun;4(2):83-93. Links

Plasma leptin concentrations are independently associated with insulin sensitivity in lean and overweight cats.

Companion Animal Sciences, School of Veterinary Science, The University of Queensland, St. Lucia, Brisbane, Australia.

This study investigated relationships between plasma leptin, insulin concentrations, insulin sensitivity and glucose tolerance in lean and overweight cats. Leptin concentrations were measured in 16 cats during glucose tolerance tests before and after gaining weight, and after feeding a test meal in overweight cats. An important finding of this study is that in both lean (r=-0.79) and overweight (r=-0.89) cats, the higher the leptin concentrations, the more insulin resistant the cat, independent of the degree of adiposity. Leptin concentrations at baseline and after consuming a meal tended to be higher in overweight cats with glucose intolerance, compared to overweight cats with normal glucose tolerance, although the difference was not significant. After feeding the test meal to overweight cats in the early morning, plasma leptin concentrations initially decreased before subsequently rising to peak 15 h later, which coincided with late evening. The leptin peak occurred 9 h after the insulin peak following ingestion of the test meal. Importantly, this study suggests that increased leptin concentrations may contribute to the diminished insulin sensitivity seen in overweight cats. Alternatively, the compensatory hyperinsulinaemia found with insulin resistance in overweight cats could stimulate leptin production. Copyright 2002 Published by Elsevier Science Ltd on behalf of ESFM and AAFP.

PMID: 12027507 [PubMed - indexed for MEDLINE]