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Titolo:
Prevention of glucoprivic stimulation of corticosterone secretion by leptin does not restore high frequency luteinizing hormone pulses in rats
Autore:
Nagatani, S; Thompson, RC; Foster, DL;
Indirizzi:
Univ Michigan, Reprod Sci Program, Ann Arbor, MI 48109 USA Univ Michigan Ann Arbor MI USA 48109 Sci Program, Ann Arbor, MI 48109 USA Univ Michigan, Dept Obstet & Gynecol, Ann Arbor, MI 48109 USA Univ Michigan Ann Arbor MI USA 48109 t & Gynecol, Ann Arbor, MI 48109 USA Univ Michigan, Dept Biol, Ann Arbor, MI 48109 USA Univ Michigan Ann ArborMI USA 48109 , Dept Biol, Ann Arbor, MI 48109 USA
Titolo Testata:
JOURNAL OF NEUROENDOCRINOLOGY
fascicolo: 4, volume: 13, anno: 2001,
pagine: 371 - 377
SICI:
0953-8194(200104)13:4<371:POGSOC>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
CORTICOTROPIN-RELEASING FACTOR; GLUCOSE AVAILABILITY; FEMALE RATS; GONADOTROPIN-SECRETION; REPRODUCTIVE FUNCTIONS; PREOPTIC AREA; RHESUS-MONKEY; OBESE OB/OB; PULSATILE; AXIS;
Keywords:
leptin; LH; glucose availability; immobilization; corticosterone;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
53
Recensione:
Indirizzi per estratti:
Indirizzo: Foster, DL Univ Michigan, Reprod Sci Program, Room 1101,300 N Ingalls Bldg, Ann Arbor, MI 48109 USA Univ Michigan Room 1101,300 N Ingalls Bldg Ann Arbor MI USA 48109
Citazione:
S. Nagatani et al., "Prevention of glucoprivic stimulation of corticosterone secretion by leptin does not restore high frequency luteinizing hormone pulses in rats", J NEUROENDO, 13(4), 2001, pp. 371-377

Abstract

We have previously determined that exogenous leptin prevents the inhibition of pulsatile luteinizing hormone (LH) release in the fasting rodent. The present study tested the hypothesis that the mechanism by which leptin facilitates high LH secretion is through an attenuation of the stress response produced by a deficit in energy. Because hypogonadotropism is associated with activation of the hypothalamic-pituitary-adrenal (HPA) axis during both metabolic stress and nonmetabolic stress, our approach included a comparison of whether exogenous leptin could prevent the rise in corticosterone produced by a nonmetabolic stress (immobilization for 2 h), as well as by a widely used metabolic stress (transient glucoprivation by 2-deoxyglucose, 2DG;400 mg/kg, b.w., i.v.). Each stressor was applied to well-fed ovariectomized rats (n = 4-6 per group), 2 h after leptin (3 mug/g, b.w., i.p.) or vehicle administration. Blood samples were collected through an indwelling atrial cannula every 6 min for 1 h before and for 2 h after the stress treatment to measure LH, leptin and corticosterone. During metabolic stress (acute glucoprivation), circulating leptin decreased, corticosterone increased andLH decreased; leptin administration abolished the increase in corticosterone, but pulsatile LH secretion remained inhibited. In contrast, during nonmetabolic stress (immobilization), leptin secretion was unaffected, but circulating corticosterone increased and LH decreased; leptin treatment did notprevent either the increase in corticosterone or the decrease in LH secretion. An important overall finding is that leptin can differentially alter the HPA axis depending upon the type of stress. In addition, whether the pattern of leptin is altered depends upon the type of stress. Although a glucoprivic-induced decrease in endogenous leptin can be a stressor responsible for the increase in corticosterone secretion, a nonmetabolic stress-inducedincrease in corticosterone is not mediated by leptin. Moreover, our results reveal that the depression of LH secretion when leptin is low during reduced energy availability is not due to activation of the HPA axis. During anenergy deficit, exogenous leptin could not restore high frequency LH secretion when HPA function was restored to normal. Finally, the inability of leptin to increase LH secretion in the face of 2DG supports the notion that the action of leptin is dependent upon the degree of glucose availability.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 18/01/20 alle ore 13:13:22