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Multiple cytokines and acute inflammation raise mouse leptin levels: potential role in inflammatory anorexia.

Sarraf P, Frederich RC, Turner EM, Ma G, Jaskowiak NT, Rivet DJ, Flier JS, Lowell BB, Fraker DL, Alexander HR - J. Exp. Med. (1997)

Bottom Line: Several inflammatory cytokines, most notably tumor necrosis factor (TNF) and IL-1, induce anorexia and loss of lean body mass, common manifestations of acute and chronic inflammatory conditions.IL-10, IL-4, ciliary neurotrophic factor, and IL-2, cytokines not known to induce anorexia or decrease food intake, had no effect on leptin gene expression or serum leptin levels.After administration of Escherichia coli lipopolysaccharide (LPS), leptin gene expression and leptin levels were increased.

View Article: PubMed Central - PubMed

Affiliation: Surgical Metabolism Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.

ABSTRACT
Several inflammatory cytokines, most notably tumor necrosis factor (TNF) and IL-1, induce anorexia and loss of lean body mass, common manifestations of acute and chronic inflammatory conditions. In C57BL/6 female mice, the administration of TNF, IL-1, and, to a lesser extent, leukemia inhibitory factor (LIF), produced a prompt and dose-dependent increase in serum leptin levels and leptin mRNA expression in fat. IL-10, IL-4, ciliary neurotrophic factor, and IL-2, cytokines not known to induce anorexia or decrease food intake, had no effect on leptin gene expression or serum leptin levels. After administration of Escherichia coli lipopolysaccharide (LPS), leptin gene expression and leptin levels were increased. These findings suggest that leptin levels may be one mechanism by which anorexia is induced during acute inflammatory conditions.

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Related in: MedlinePlus

Leptin levels in freely feeding mice at intervals throughout a  24-h period and after short-term fasting and refeeding. The initial point  represents midnight, 5.5 h after beginning the dark cycle in the ad libitum  fed diurnal experiment, 7 h after the commencement of the fast in the  fasting and refeeding experiments, and the beginning of refeeding in the  latter experiment. Each point represents the mean ± SEM of 6–8 individually measured mice. Northern blot shows ob gene expression in adipose  tissue from freely fed mice (control), decreased expression after a 7- or 12-h  fast (starved), and increased 5 h after refeeding groups of mice starved for 7 h  (refed 5 h).
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Figure 1: Leptin levels in freely feeding mice at intervals throughout a 24-h period and after short-term fasting and refeeding. The initial point represents midnight, 5.5 h after beginning the dark cycle in the ad libitum fed diurnal experiment, 7 h after the commencement of the fast in the fasting and refeeding experiments, and the beginning of refeeding in the latter experiment. Each point represents the mean ± SEM of 6–8 individually measured mice. Northern blot shows ob gene expression in adipose tissue from freely fed mice (control), decreased expression after a 7- or 12-h fast (starved), and increased 5 h after refeeding groups of mice starved for 7 h (refed 5 h).

Mentions: We first examined the characteristics of leptin gene expression and serum levels under simple physiological manipulations, including circadian variation in freely feeding mice and the response to acute starvation and refeeding. As previously demonstrated at the mRNA level (25), leptin levels under conditions of ad libitum feeding were lowest in the middle of light cycle and highest in the middle of the dark cycle (Fig. 1), consistent with the well-established diurnal but primarily nocturnal food intake behavior of rodents (26). When animals were fasted beginning 2 h before the night cycle, the nocturnal rise was abolished. When 7-h fasted animals were refed, there was an exuberant increase in leptin gene expression and serum levels higher than freely fed controls and were manifest as early as 3 h after feeding (Fig. 1).


Multiple cytokines and acute inflammation raise mouse leptin levels: potential role in inflammatory anorexia.

Sarraf P, Frederich RC, Turner EM, Ma G, Jaskowiak NT, Rivet DJ, Flier JS, Lowell BB, Fraker DL, Alexander HR - J. Exp. Med. (1997)

Leptin levels in freely feeding mice at intervals throughout a  24-h period and after short-term fasting and refeeding. The initial point  represents midnight, 5.5 h after beginning the dark cycle in the ad libitum  fed diurnal experiment, 7 h after the commencement of the fast in the  fasting and refeeding experiments, and the beginning of refeeding in the  latter experiment. Each point represents the mean ± SEM of 6–8 individually measured mice. Northern blot shows ob gene expression in adipose  tissue from freely fed mice (control), decreased expression after a 7- or 12-h  fast (starved), and increased 5 h after refeeding groups of mice starved for 7 h  (refed 5 h).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2196098&req=5

Figure 1: Leptin levels in freely feeding mice at intervals throughout a 24-h period and after short-term fasting and refeeding. The initial point represents midnight, 5.5 h after beginning the dark cycle in the ad libitum fed diurnal experiment, 7 h after the commencement of the fast in the fasting and refeeding experiments, and the beginning of refeeding in the latter experiment. Each point represents the mean ± SEM of 6–8 individually measured mice. Northern blot shows ob gene expression in adipose tissue from freely fed mice (control), decreased expression after a 7- or 12-h fast (starved), and increased 5 h after refeeding groups of mice starved for 7 h (refed 5 h).
Mentions: We first examined the characteristics of leptin gene expression and serum levels under simple physiological manipulations, including circadian variation in freely feeding mice and the response to acute starvation and refeeding. As previously demonstrated at the mRNA level (25), leptin levels under conditions of ad libitum feeding were lowest in the middle of light cycle and highest in the middle of the dark cycle (Fig. 1), consistent with the well-established diurnal but primarily nocturnal food intake behavior of rodents (26). When animals were fasted beginning 2 h before the night cycle, the nocturnal rise was abolished. When 7-h fasted animals were refed, there was an exuberant increase in leptin gene expression and serum levels higher than freely fed controls and were manifest as early as 3 h after feeding (Fig. 1).

Bottom Line: Several inflammatory cytokines, most notably tumor necrosis factor (TNF) and IL-1, induce anorexia and loss of lean body mass, common manifestations of acute and chronic inflammatory conditions.IL-10, IL-4, ciliary neurotrophic factor, and IL-2, cytokines not known to induce anorexia or decrease food intake, had no effect on leptin gene expression or serum leptin levels.After administration of Escherichia coli lipopolysaccharide (LPS), leptin gene expression and leptin levels were increased.

View Article: PubMed Central - PubMed

Affiliation: Surgical Metabolism Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.

ABSTRACT
Several inflammatory cytokines, most notably tumor necrosis factor (TNF) and IL-1, induce anorexia and loss of lean body mass, common manifestations of acute and chronic inflammatory conditions. In C57BL/6 female mice, the administration of TNF, IL-1, and, to a lesser extent, leukemia inhibitory factor (LIF), produced a prompt and dose-dependent increase in serum leptin levels and leptin mRNA expression in fat. IL-10, IL-4, ciliary neurotrophic factor, and IL-2, cytokines not known to induce anorexia or decrease food intake, had no effect on leptin gene expression or serum leptin levels. After administration of Escherichia coli lipopolysaccharide (LPS), leptin gene expression and leptin levels were increased. These findings suggest that leptin levels may be one mechanism by which anorexia is induced during acute inflammatory conditions.

Show MeSH
Related in: MedlinePlus