Leptin Reduces Body Weight Gain in Neonatal Rats

Yuan, Chun‐Su; Attele, Anoja S.; Zhang, Liu; Lynch, James P.; Xie, Jing‐Tian; Shi, Zhi Qing

doi:10.1203/00006450-200009000-00021

Cited by 34 publications

(31 citation statements)

References 31 publications

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“…We observed a reduction in the body weight of artificially reared vs sow-reared piglets; however, in contrast to previous studies in neonatal rats (Yuan et al 2000), we did not observe body weight reduction following leptin treatment. This can be related to either the much higher doses of leptin applied and/or different route of leptin administration (i.p.)…”

Section: Discussioncontrasting

confidence: 99%

Exogenous leptin controls the development of the small intestine in neonatal piglets

Woliński¹,

Biernat²,

Guilloteau³

et al. 2003

Journal of Endocrinology

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Leptin, a hormone produced and secreted by adipose tissue, muscles and stomach, is involved in the regulation of adipose tissue mass, food intake and body weight in neonatal animals. It is also produced in the mammary glands and secreted into the colostrum and milk. Since leptin receptors are widely distributed in the small intestine mucosa, the aim of the present study was to investigate the effect of exogenous leptin on the development of the small intestine in neonatal piglets. Male neonatal piglets were fed with sow's milk or artificial milk formula. Every 8 h the latter received either vehicle or leptin (2 or 10 µg/kg body weight). The animals were either killed after 6 days of treatment and the small intestine sampled for histology and brush border enzyme activities or were tested for marker molecule (Na-fluorescein and BSA) absorption in vivo. Feeding milk formula slowed the maturation of small intestinal mucosa compared with feeding sow's milk. However, after leptin treatment the length of the small intestine was increased, and intestinal villi length, but not crypt size, was reduced compared with controls. The mitotic index was increased and the percentage of vacuolated enterocytes was reduced in the entire small intestine. Enterocyte brush border protease and lactase activities were reduced in the jejunum. Nafluorescein marker molecule absorption did not change but that of BSA was reduced 3·8-fold. In conclusion, exogenous leptin administered in physiological doses reversed the maturation of the small intestinal mucosa to the range found in sow-reared piglets.

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Section: Discussioncontrasting

confidence: 99%

Exogenous leptin controls the development of the small intestine in neonatal piglets

Woliński¹,

Biernat²,

Guilloteau³

et al. 2003

Journal of Endocrinology

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“…Thus at 3 days of age, exogenous Dex may have increased adipocytic production of leptin while suppressing endogenous corticosterone concentrations. Hyperleptinemia can suppress hypothalamic NPY concentrations and diminish milk intake (1,6,51). This decrease in calorie intake can potentially initiate postnatal growth retardation (51).…”

Section: Day Oldmentioning

confidence: 99%

Postnatal glucocorticoid exposure alters the adult phenotype

He¹,

Varma²,

Weissfeld³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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He, Jing, Amit Varma, Lisa A. Weissfeld, and Sherin U. Devaskar. Postnatal glucocorticoid exposure alters the adult phenotype. Am J Physiol Regul Integr Comp Physiol 287: R198 -R208, 2004. First published March 4, 2004 10.1152/ajpregu.00349.2003We examined the effect of six doses of dexamethasone (Dex) administered daily (2-7 days of age) to postnatal rats on body weight gain, food and water intake, peripheral hormonal/metabolic milieu, and hypothalamic neuropeptides that regulate food intake. We observed a Dex-induced acute (3 days of age) suppression of endogenous corticosterone and an increase in circulating leptin concentrations that were associated with a decrease in body weight in males and females. Followup during the suckling, postsuckling, and adult stages (7-120 days of age) revealed hypoleptinemia in males and females, and hypoinsulinemia, a relative increase in the glucose-to-insulin ratio, and a larger increase in skeletal muscle glucose transporter (GLUT 4) concentrations predominantly in the males, reflective of a catabolic state associated with a persistent decrease in body weight gain. The increase in the glucose-to-insulin ratio and hyperglycemia was associated with an increase in water intake. In addition, the changes in the hormonal/metabolic milieu were associated with an increase in hypothalamic neuropeptide Y content in males and females during the suckling phase, which persisted only in the 120-day-old female with a transient postnatal decline in ␣-melanocyte-stimulating hormone and corticotropin-releasing factor. This increase in neuropeptide Y (NPY) during the suckling phase in males and females was associated with a subsequent increase in adult food intake that outweighed the demands of body weight gain. In contrast to the adult hypothalamic findings, cerebral ventricular dilatation was more prominent in adult males. We conclude that postnatal Dex treatment causes permanent sex-specific changes in the adult phenotype, setting the stage for future development of diabetes (increased glucose:insulin ratio), obesity (increased NPY and food intake), and neurological impairment (loss of cerebral volume). development; food intake; neuropeptide Y; glucose transporters POSTNATAL GLUCOCORTICOID THERAPY constituted a standard intervention to combat chronic lung disease in the newborn premature infant (18,40). Recent reports of adverse outcomes such as cerebral palsy have cautioned the clinicians into judicious use of this drug (2, 17, 50). However, there still continue to be certain infants with chronic lung changes who are resilient to conventional modes of therapy warranting the use of postnatal glucocorticoids as a life-saving intervention (19,42). Furthermore, despite the absence of well-controlled trials, glucocorticoids are still used in term infants for differing indications other than prevention of chronic lung disease. While the adverse effects of antenatal glucocorticoid therapy have been examined and long-term changes reported in animals (13,20,33,37,38), limited studies exist in resp...

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“…Plasma leptin appears to remain low after birth (16), and in rat pups, leptin treatments are known to induce weight loss and adipose tissue mobilization (17). It is possible that peripheral levels of leptin are maintained at low levels after birth to ensure that the neonate's appetite is high and adipose tissue deposition is maximized.…”

mentioning

confidence: 99%