Elevated serum leptin concentrations induced by experimental acute inflammation

Gualillo, Oreste; Eiras, Sonia; Lago, Francisca; Diéguez, Carlos; Casanueva, Felipe F.

doi:10.1016/s0024-3205(00)00827-4

Cited by 126 publications

(89 citation statements)

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“…Leptin expression is not only regulated by the intake of food, but also by various hormones, as well as by several inflammatory mediators [85][86]. In general, serum leptin levels directly correlate with insulin levels and inversely correlate with glucocorticoid levels, and increase in the course of acute infection and sepsis [85,[87][88].…”

Section: Leptin and Inflammationmentioning

confidence: 99%

Leptin and Inflammation

Iikuni¹,

Lam²,

Lu³

et al. 2008

CIR

303

251

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The past few years of research on leptin have provided important information on the link between metabolism and immune homeostasis. Adipocytes influence not only the endocrine system but also the immune response through several cytokine-like mediators known as adipokines, which include leptin. It is widely accepted that leptin can directly link nutritional status and pro-inflammatory T helper 1 immune responses, and that a decrease of leptin plasma concentration during food deprivation can lead to an impaired immune function. Additionally, several studies have implicated leptin in the pathogenesis of chronic inflammation, and the elevated circulating leptin levels in obesity appear to contribute to the low-grade inflammatory background which makes obese individuals more susceptible to increased risk of developing cardiovascular diseases, type II diabetes, or degenerative disease including autoimmunity and cancer. Conversely, reduced levels of leptin such as those found in malnourished individuals have been linked to increased risk of infection and reduced cell-mediated immune responses. We discuss here the functional influences of leptin in the physiopathology of inflammation, and the effects of leptin in the modulation of such responses.

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Section: Leptin and Inflammationmentioning

confidence: 99%

Leptin and Inflammation

Iikuni¹,

Lam²,

Lu³

et al. 2008

CIR

303

251

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“…It decreases food intake and increases energy consumption by acting on hypothalamic nuclei, inducing anorexigenic factors cocaine amphetamine related transcript (CART), pro-opiomelanocortin and suppressing orexigenic neuropeptides such as neuropeptide Y, agouti related protein, and orexin (Ahima et al 1996). Leptin levels are mainly dependent on the amount of body fat, but its synthesis is also regulated by sex hormones and a wide range of inflammation mediators (Sarraf et al 1997, Gualillo et al 2000. As a result of the effects of sex hormones, leptin levels are higher in women than in men even when adjusted for body mass index, which may be relevant to the influence of sex on the development or frequency of certain diseases, such as osteoarthritis (Blum et al 1997, Teichtahl et al 2005.…”

Section: Leptin: the Harbingermentioning

confidence: 99%

Adipokines in the skeleton: influence on cartilage function and joint degenerative diseases

Gómez

Lago²,

Gómez-Reino³

et al. 2009

Journal of Molecular Endocrinology

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The discovery of leptin in 1994 marked the beginning of a new understanding about white adipose tissue (WAT) and modified a static vision of this tissue which was viewed up to the end of the 20th century as an inert tissue, devoted to body protection from heat loss and to passively storing energy. The identification of the product of the gene obese accentuated the role of adipose tissue in the physiopathology of obesity-linked diseases, and led to the discovery of various adipokines, many of a pro-inflammatory nature. It has become progressively manifest that WAT-derived adipokines can now be considered as the fulcrum between obesity-related environmental causes, such as nutrition and lifestyle, and the biochemical shifts that lead to metabolic syndrome, inflammatory and/or autoimmune conditions, and rheumatic diseases. Herein, we review recent adipokine research, with particular emphasis to the role of leptin, adiponectin, resistin, and visfatin in chondrocyte function and skeleton, as well as in inflammatory and degenerative cartilage joint diseases.

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“…It is now known that: (i) a rise in plasma leptin may occur as early as 1 h post-LPS; (ii) the rise may last for several hours; (iii) the magnitude of the rise is directly proportional to the LPS dose until a ceiling level of leptin is reached; (iv) as in non-inflammatory states, the ceiling level of leptin is ∼20 ng/ml in lean animals, but it may be higher in obese animals; and (v) the leptin response to LPS occurs in both fasted and fed animals, but the peak leptin level achieved in fasted animals is lower, possibly due to their already reduced basal production of leptin. Inflammatory stimuli other than LPS, specifically turpentine [84] and carrageenan [91], also stimulate leptin production. It is not surprising, therefore, that plasma leptin was found to be high in mice and humans with bacterial sepsis [92,93] as well as in those patients who developed post-surgical inflammation [94].…”

Section: Leptin Production In Inflammationmentioning

confidence: 99%

Leptin: At the crossroads of energy balance and systemic inflammation

Steiner

Romanovsky

2007

Progress in Lipid Research

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In addition to playing a central role in energy homeostasis, leptin is also an important player in the inflammatory response. Systemic inflammation is accompanied by fever (less severe cases) or hypothermia (more severe cases). In leptin-irresponsive mutants, the hypothermia of systemic inflammation is exaggerated, presumably due to the enhanced production and cryogenic action of tumor necrosis factor (TNF)-α. Mechanisms that exaggerate hypothermia can also attenuate fever, particularly in a cool environment. Another common manifestation of systemic inflammation is behavioral depression. Along with the production of interleukin (IL)-1β, this manifestation is exaggerated in leptin-irresponsive mutants. The enhanced production of TNF-α and IL-1β may be due, at least in part, to insufficient activation of the anti-inflammatory hypothalamo-pituitary-adrenal axis by immune stimuli in the absence of leptin signaling. In experimental animals and humans that are responsive to leptin, suppression of leptin production under conditions of negative energy balance (e.g., fasting) can exaggerate both hypothermia and behavioral depression. Since these manifestations aid energy conservation, exaggeration of these manifestations under conditions of negative energy balance is likely to be beneficial.

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Elevated serum leptin concentrations induced by experimental acute inflammation

Cited by 126 publications

References 0 publications

Leptin and Inflammation

Leptin and Inflammation

Adipokines in the skeleton: influence on cartilage function and joint degenerative diseases

Leptin: At the crossroads of energy balance and systemic inflammation

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