Serum leptin levels in acute protein deprivation

Philip P. Stapleton, Catherine B. Barden, Martin D. McCarter, Peter J. Mackrell, Tracy A. Freeman, Hassan A. Naama, John M. Daly

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Background: Protein energy malnutrition (PEM) induces a host neuroendocrine response, reflected by significant elevations in circulating glucocorticoid levels and associated with metabolic and immune dysfunction. Leptin regulates food intake and body mass and has a significant impact on the hypothalamic-pituitary-adrenal axis (HPA). We hypothesized that leptin may be altered by and may play an important role in regulating the effects of PEM. Methods: Female Balb/c mice were used. In experiment 1, mice were pair-fed either a protein-free (0% casein) or control (24% casein) diet for 7 days. In experiment 2, mice were implanted with either a placebo or corticosterone-releasing pellet and fed the control diet for 7 days. In experiment 3, adrenalectomized mice were pair-fed either the protein-free or control diet for 7 days. Serum corticosterone and leptin levels were measured in all experiments. Results: PEM caused significant reductions in food intake, body weight, and total body fat, but not lean body mass. Serum corticosterone and leptin levels were significantly greater in mice fed the protein-free diet. Subcutaneous implantation of a corticosterone pellet in mice fed the control diet resulted in a significantly elevated serum leptin level compared with placebo-implanted controls. Bilateral adrenalectomy partially blunted the increased serum leptin in PEM. Conclusions: Leptin may be an important mediator of weight loss and decreased food intake in PEM. Elevated serum leptin in PEM may be secondary to elevated serum corticosterone, with other factors inherent in the host response to protein restriction also contributing to elevated serum leptin.

Original languageEnglish (US)
Pages (from-to)132-136
Number of pages5
JournalJournal of Parenteral and Enteral Nutrition
Volume27
Issue number2
StatePublished - Mar 2003

Fingerprint

Leptin
leptin
Protein-Energy Malnutrition
protein energy malnutrition
corticosterone
Corticosterone
Serum
Proteins
proteins
mice
Diet
food intake
diet
Eating
Caseins
placebos
pellets
casein
Placebos
Protein-Restricted Diet

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Food Science

Cite this

Stapleton, P. P., Barden, C. B., McCarter, M. D., Mackrell, P. J., Freeman, T. A., Naama, H. A., & Daly, J. M. (2003). Serum leptin levels in acute protein deprivation. Journal of Parenteral and Enteral Nutrition, 27(2), 132-136.

Serum leptin levels in acute protein deprivation. / Stapleton, Philip P.; Barden, Catherine B.; McCarter, Martin D.; Mackrell, Peter J.; Freeman, Tracy A.; Naama, Hassan A.; Daly, John M.

In: Journal of Parenteral and Enteral Nutrition, Vol. 27, No. 2, 03.2003, p. 132-136.

Research output: Contribution to journalArticle

Stapleton, PP, Barden, CB, McCarter, MD, Mackrell, PJ, Freeman, TA, Naama, HA & Daly, JM 2003, 'Serum leptin levels in acute protein deprivation', Journal of Parenteral and Enteral Nutrition, vol. 27, no. 2, pp. 132-136.
Stapleton PP, Barden CB, McCarter MD, Mackrell PJ, Freeman TA, Naama HA et al. Serum leptin levels in acute protein deprivation. Journal of Parenteral and Enteral Nutrition. 2003 Mar;27(2):132-136.
Stapleton, Philip P. ; Barden, Catherine B. ; McCarter, Martin D. ; Mackrell, Peter J. ; Freeman, Tracy A. ; Naama, Hassan A. ; Daly, John M. / Serum leptin levels in acute protein deprivation. In: Journal of Parenteral and Enteral Nutrition. 2003 ; Vol. 27, No. 2. pp. 132-136.
@article{adbc457547654b658fbd11ac3a3d4608,
title = "Serum leptin levels in acute protein deprivation",
abstract = "Background: Protein energy malnutrition (PEM) induces a host neuroendocrine response, reflected by significant elevations in circulating glucocorticoid levels and associated with metabolic and immune dysfunction. Leptin regulates food intake and body mass and has a significant impact on the hypothalamic-pituitary-adrenal axis (HPA). We hypothesized that leptin may be altered by and may play an important role in regulating the effects of PEM. Methods: Female Balb/c mice were used. In experiment 1, mice were pair-fed either a protein-free (0{\%} casein) or control (24{\%} casein) diet for 7 days. In experiment 2, mice were implanted with either a placebo or corticosterone-releasing pellet and fed the control diet for 7 days. In experiment 3, adrenalectomized mice were pair-fed either the protein-free or control diet for 7 days. Serum corticosterone and leptin levels were measured in all experiments. Results: PEM caused significant reductions in food intake, body weight, and total body fat, but not lean body mass. Serum corticosterone and leptin levels were significantly greater in mice fed the protein-free diet. Subcutaneous implantation of a corticosterone pellet in mice fed the control diet resulted in a significantly elevated serum leptin level compared with placebo-implanted controls. Bilateral adrenalectomy partially blunted the increased serum leptin in PEM. Conclusions: Leptin may be an important mediator of weight loss and decreased food intake in PEM. Elevated serum leptin in PEM may be secondary to elevated serum corticosterone, with other factors inherent in the host response to protein restriction also contributing to elevated serum leptin.",
author = "Stapleton, {Philip P.} and Barden, {Catherine B.} and McCarter, {Martin D.} and Mackrell, {Peter J.} and Freeman, {Tracy A.} and Naama, {Hassan A.} and Daly, {John M.}",
year = "2003",
month = "3",
language = "English (US)",
volume = "27",
pages = "132--136",
journal = "Journal of Parenteral and Enteral Nutrition",
issn = "0148-6071",
publisher = "SAGE Publications Inc.",
number = "2",

}

TY - JOUR

T1 - Serum leptin levels in acute protein deprivation

AU - Stapleton, Philip P.

AU - Barden, Catherine B.

AU - McCarter, Martin D.

AU - Mackrell, Peter J.

AU - Freeman, Tracy A.

AU - Naama, Hassan A.

AU - Daly, John M.

PY - 2003/3

Y1 - 2003/3

N2 - Background: Protein energy malnutrition (PEM) induces a host neuroendocrine response, reflected by significant elevations in circulating glucocorticoid levels and associated with metabolic and immune dysfunction. Leptin regulates food intake and body mass and has a significant impact on the hypothalamic-pituitary-adrenal axis (HPA). We hypothesized that leptin may be altered by and may play an important role in regulating the effects of PEM. Methods: Female Balb/c mice were used. In experiment 1, mice were pair-fed either a protein-free (0% casein) or control (24% casein) diet for 7 days. In experiment 2, mice were implanted with either a placebo or corticosterone-releasing pellet and fed the control diet for 7 days. In experiment 3, adrenalectomized mice were pair-fed either the protein-free or control diet for 7 days. Serum corticosterone and leptin levels were measured in all experiments. Results: PEM caused significant reductions in food intake, body weight, and total body fat, but not lean body mass. Serum corticosterone and leptin levels were significantly greater in mice fed the protein-free diet. Subcutaneous implantation of a corticosterone pellet in mice fed the control diet resulted in a significantly elevated serum leptin level compared with placebo-implanted controls. Bilateral adrenalectomy partially blunted the increased serum leptin in PEM. Conclusions: Leptin may be an important mediator of weight loss and decreased food intake in PEM. Elevated serum leptin in PEM may be secondary to elevated serum corticosterone, with other factors inherent in the host response to protein restriction also contributing to elevated serum leptin.

AB - Background: Protein energy malnutrition (PEM) induces a host neuroendocrine response, reflected by significant elevations in circulating glucocorticoid levels and associated with metabolic and immune dysfunction. Leptin regulates food intake and body mass and has a significant impact on the hypothalamic-pituitary-adrenal axis (HPA). We hypothesized that leptin may be altered by and may play an important role in regulating the effects of PEM. Methods: Female Balb/c mice were used. In experiment 1, mice were pair-fed either a protein-free (0% casein) or control (24% casein) diet for 7 days. In experiment 2, mice were implanted with either a placebo or corticosterone-releasing pellet and fed the control diet for 7 days. In experiment 3, adrenalectomized mice were pair-fed either the protein-free or control diet for 7 days. Serum corticosterone and leptin levels were measured in all experiments. Results: PEM caused significant reductions in food intake, body weight, and total body fat, but not lean body mass. Serum corticosterone and leptin levels were significantly greater in mice fed the protein-free diet. Subcutaneous implantation of a corticosterone pellet in mice fed the control diet resulted in a significantly elevated serum leptin level compared with placebo-implanted controls. Bilateral adrenalectomy partially blunted the increased serum leptin in PEM. Conclusions: Leptin may be an important mediator of weight loss and decreased food intake in PEM. Elevated serum leptin in PEM may be secondary to elevated serum corticosterone, with other factors inherent in the host response to protein restriction also contributing to elevated serum leptin.

UR - http://www.scopus.com/inward/record.url?scp=0037373027&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0037373027&partnerID=8YFLogxK

M3 - Article

C2 - 12665169

AN - SCOPUS:0037373027

VL - 27

SP - 132

EP - 136

JO - Journal of Parenteral and Enteral Nutrition

JF - Journal of Parenteral and Enteral Nutrition

SN - 0148-6071

IS - 2

ER -