Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 17

Liczba wyników na stronie
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników

Wyniki wyszukiwania

help Sortuj według:

help Ogranicz wyniki do:
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
Leptin and glucagon-like peptide-1 (GLP-1) were proved to act in concert to control the activity of feeding centres. Since leptin receptor was identified in the gut endocrine L cells and neurons producing GLP-1, we have checked whether GLP-1 mediates the effects of leptin on feeding and drinking behaviour. To this aim, an intraperitoneal or intracerebroventricular injection of exendin (9 - 39), a GLP-1 antagonist, (50 or 10 µg per rat, respectively) followed by leptin (100 or 5 µg per rat, respectively) was made and 24-hour food intake and body weight changes were measured. Previous injection of exendin (9 - 39) completely abolished the suppressory effect of peripheral leptin on food intake and body weight gain. Moreover, exendin (9 - 39) significantly attenuated the effect of intracerebroventricular leptin on food but not water consumption. It is concluded that intact GLP-1 signalling is necessary to mediate the effect of leptin on food intake in the rat. Conversely, leptin seems to affect the thirst center function independently of GLP-1. Also, these findings produce further evidence for close interactions between long- and short-term factors regulating the activity of feeding centres.
Feeding behavior is closely related to the circadian activity of humans and animals. The endocannabinoid system is known to affect the circadian changes in energy balance and gastrointestinal peptides were found to change the expression of CB1 receptor in vagal terminals in the alimentary tract. Therefore, we have examined whether the anorectic action of CB1 receptor antagonist, AM 251, may be modified by activation or blockade of GLP-1 receptor. Male Wistar rats were housed in individual cages and maintained on a 12:12 hour light-dark cycle with free access to standard, pelleted rat chow and water. Each rat received a preweighed amount of food every day throughout the experiment. The animals were injected intraperitoneally either with a CB1 receptor antagonist, AM251 (2 mg/kg bw.), followed 15 min later by a GLP-1 antagonist, exendin (9-39) (160 µg/kg bw.), or AM 251 (1 mg/kg bw.) followed 15 min later by a GLP-1 agonist, exendin 4 (1.5 µg/kg bw.). All injections were made 1 – 1.5 hour before lights off. 24-hour food intake was recorded two days before and two days after the injection. AM 251 at a dose of 2 mg/kg significantly reduced daily food intake and concomitant injection of exendin (9-39), at a dose found previously to prevent the action of other anorectic agents, had no effect on a AM 251-induced decrease in food consumption. On the other hand, either 1 mg/kg AM 251 or 1.5 µg exendin-4 administered alone had no significant effect on 24-hour food intake. When, however, these drugs were co-injected, a marked reduction in 24-hour food intake occurred. These results indicate that (1) the anorectic action of CB1 receptor antagonist is not mediated by GLP-1 and (2) the CB1 receptor antagonist and GLP-1 receptor agonist act synergistically to reduce the daily food consumption in the rat when injected before of the nocturnal feeding phase. This work was supported by the National Centre for Science (grant No. 0056/B/ P01/2011/40).
Bojanowska E. and Guzek J. W.: Iloprost (ZK 36374; a stable prostacyclin analogue) increases basal as well as potassium-evoked vasopressin and oxytocin secretion from rat neurointermediate lobes in vitro. This finding suggests a possible regulatory role of endogenous prostacyclin in the release of neurohypophysial hormones.
Leptin interplays with other peptides to control feeding behaviour in humans and animals. Using exendin-4, an agonist of glucagon-like peptide-1, we investigated whether leptin modifies its effect on food intake in the rat. In the first series, exendin-4 alone (0.1, 2 or 10 µg per rat), leptin alone (0.1, 2, 10 or 100 µg per rat) or exendin-4 and leptin together (0.1 + 0.1, 2 + 2, 10 + 10, or 2 + 100 µg per rat, respectively) were injected once intraperitoneally. In the second series animals were injected either with exendin-4 (2 µg) alone, leptin (10 µg) alone, or leptin (10 µg) + exendin-4 (2 µg) daily for 5 subsequent days. At the lowest dose used, leptin and exendin-4 injected once together, but not separately, reduced significantly a 24-hour food intake. When used in higher doses, however, leptin did not change the exendin-4-dependent suppressory effect on food consumption. No significant differences in food intake were seen between rats treated repeatedly with exendin-4 only and animals injected with both drugs. Hence, leptin and exendin-4 may act additively to inhibit appetite when present in low concentrations while, at high leptin doses, this effect is abolished. The lack of synergistic effects of exendin-4 and high leptin concentrations on food intake may explain, at least in part, mechanisms responsible for leptin resistance in subjects with hyperleptinaemia.
To date, glucagon-like peptide–1 (7-36) amide (tGLP-1) has been found to enhance the vasopressin and oxytocin secretion in vivo but not in vitro (i.e., when the isolated neurointermediate lobe of the pituitary was used for experiments). The goal of this study was to investigate whether tGLP-1 can influence the function of the hypothalamo-neurohypophysial complex in vitro. Also, the effect of a tGLP-1 agonist, exendin-4, and antagonist, exendin-(9-39), on the release of vasopressin/oxytocin from the isolated rat hypothalamo-neurohypophysial complex was tested. tGLP-1 enhanced the basal but not the potassium-stimulated release of vasopressin and oxytocin from the hypothalamo-neurohypophysial complex. On the other hand, tGLP-1 failed to affect the release of both hormones from the isolated neurointermediate lobe. The tGLP-1 agonist increased the secretion of oxytocin and vasopressin from the hypothalamo-neurohypophysial system whilst the tGLP-1 antagonist completely abolished the stimulatory effect of tGLP-1 on the secretion of both hormones. It is concluded that tGLP-1 affects the function of vasopressin- and oxytocinergic neurones through specific hypothalamic receptors.
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.