Involvement of plasma leptin, insulin and free tryptophan in cytokine-induced anorexia

Sato, Tomoi; Laviano, Alessandro; Meguid, Michael M.; Chen, C.; Fanelli, Filippo Rossi; Hatakeyama, Katsuyoshi

doi:10.1054/clnu.2002.0609

Cited by 31 publications

(25 citation statements)

References 43 publications

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“…This notion is supported byLPS-induced anorexia being attenuated in insulin-deficient STZ-injected rats, which was reversed by insulin treatment. Previous study also suggests that insulin, but not leptin, may partly contribute to the anorexia of cytokines [41], and a recent study has shown that LPS increases the transport of insulin through the blood brain barrier by about three fold [42]. Therefore insulin is a possible candidate for LPS-induced anorexia in rats.…”

Section: Discussionmentioning

confidence: 87%

“…Several previous studies have reported increased plasma leptin concentration and/ or expression of the leptin gene in LPS-treated rats [28,45]. However, evidence against the essential role of leptin in LPS-induced anorexia also reported that plasma leptin levels remained unchanged or reduced in LPS-treated or cytokine-treated rats, even though food intake had been clearly reduced in male rats [41,46]. Furthermore, the induction of a food intake reduction by LPS in genetically leptin or leptin receptor-aberrant rat and mice models is not supportive of leptin's role in LPS-induced anorexia [22,23].…”

Section: Discussionmentioning

confidence: 95%

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Time-Course Changes of Hormones and Cytokines by Lipopolysaccharide and Its Relation with Anorexia

Kim

Ahn

et al. 2007

J. Physiol. Sci

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Abstract:We assessed the time course effects of lipopolysaccaride (LPS) on food intake, cytokines, and hormones in rats and evaluated the relation between LPS-induced anorexia and its possible causative factors. Food intake was reduced 2 h after LPS injection (500 µg/kg, intraperitoneally) and remained decreased for 24 h. Plasma TNF-α and IL-6 levels increased by LPS administration at 0.5 and 2 h, and at 2 and 4 h, respectively. Plasma leptin and glucose levels were elevated at 8 and 16 h, and insulin levels were elevated at 2, 4, 8, and 16 h in the LPSinjected group, as compared to the counterpart controls. IL-6 levels in the CSF were elevated at 2 and 4 h. Hypothalamic cytokines tended to increase as early as 0.5 h after LPS injection and remained increased until 16 h. LPS-induced anorexia was attenuated in insulin-deficient STZ rats and was abolished by insulin treatment. The hypothalamic expression of NPY, a target of insulin's anorexic effect, was decreased 2 h after LPS administration, and central NPY injection (3 nM) prevented LPS-induced anorexia. In conclusion, cytokines, insulin, and leptin levels evidence different time courses by LPS administration. In LPS-induced anorexia, insulin may constitute a newly found causative factor, whereas leptin appears to be uninvolved in an early period in rats.

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Section: Discussionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 95%

Time-Course Changes of Hormones and Cytokines by Lipopolysaccharide and Its Relation with Anorexia

Kim

Ahn

et al. 2007

J. Physiol. Sci

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“…It has been shown that acute inflammation and proinflammatory cytokines, such as TNF-a, IL-1, IL-6 and leucocyte inhibitory factor, positively regulate leptin expression in adipose tissue and circulating leptin levels, 24,60 whereas long-term exposure to IL-1 or TNF-a negatively regulates leptin levels. 24,61 LEPTIN IN IMMUNO-RHEUMATOLOGICAL DISEASES Autoimmunity results from a failure or breakdown of the mechanisms responsible for maintaining self-tolerance in B cells, T cells, or both cell types. Self-tolerance may be induced in generative lymphoid organs as a consequence of immature self-reactive lymphocytes recognizing self-antigens, called central tolerance, or in peripheral sites as a result of mature self-reactive lymphocytes encountering self-antigens during particular conditions, called peripheral tolerance.…”

Section: Leptin and Autoimmunity M Vadacca Et Al 205mentioning

confidence: 99%

Leptin in immuno-rheumatological diseases

et al. 2011

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Leptin is one of the most important hormones secreted by adipocytes, with a variety of physiological roles related to the control of metabolism and energy homeostasis. Since its discovery in 1994, leptin has attracted increasing interest in the scientific community for its pleiotropic actions. One of these functions is the relationship between nutritional status and immune competence. It structurally resembles proinflammatory cytokines, such as IL-6 and IL-12. The cytokine-like structural characteristic of leptin is implicative of its function in regulating immune responses. The role of leptin in regulating immune responses has been assessed in vitro as well as in clinical studies. It has been shown that disease conditions of reduced leptin production are associated with increased infection susceptibility. Conversely, immune-mediated disorders, such as autoimmune diseases, are associated with the increased secretion of leptin and the production of proinflammatory pathogenic cytokines. In this paper, we review the most recent advances of the role of leptin in immune-rheumatological diseases, and we discuss whether strategies aimed at modifying leptin levels could represent innovative and therapeutic tools for autoimmune disorders. Keywords: adipokines; autoimmune diseases; leptin; rheumatic diseases INTRODUCTIONThe existence of a factor secreted by white adipose tissue (WAT), which acts to control feeding, weight and WAT mass, was first proposed by Kennedy 1 and is supported by monogenic mutations resulting in obesity. [2][3][4] WAT is composed of adipocytes filled mainly with triacylglycerol and embedded in loose connective tissue containing adipocyte precursors, fibroblasts, immune and other cells. Obesity, the condition that originally motivated the research on WAT, is characterized by low-grade systemic inflammation. It is thought that excess WAT can contribute to the maintenance of obesity through inflammation-inducing lipotoxicity by secreting factors that stimulate the synthesis of inflammatory agents in other organs and by secreting inflammatory agents itself. 5 The current view of WAT states that it is an active contributor to body homeostasis by sending out and responding to signals that modulate appetite, energy expenditure, insulin sensitivity, the endocrine and reproductive systems, bone metabolism, inflammation and immunity. 6 Several findings have converged to indicate that adipocytes share certain properties with immune cells, such as complement activation 7 and proinflammatory cytokine production. 8 Fat cell precursors also share features with macrophages. Numerous genes that code for transcription factors, cytokines, inflammatory signaling molecules, and fatty acid transporters are essential for adipocyte biology and are also expressed and functional in macrophages. 9 Adipose tissue secrets a variety of factors: the term 'adipokine' is generally given to any protein that can be synthesized and secreted by adipocytes. Among these factors, only leptin and adiponectin (and possibly resistin, adipsi...

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“…Peripheral infusion of IL-1 induces anorexia and raises brain tryptophan levels, thereby suggesting increased serotonin synthesis (79). Interleukin-1 intrahypothalamic injection depresses food intake and increases release of serotonin (91).…”

Section: Hypothalamic Serotonergic Activity and Its Interplay With Prmentioning

confidence: 99%

Neural control of the anorexia-cachexia syndrome

Laviano¹,

Inui²,

Marks³

et al. 2008

American Journal of Physiology-Endocrinology and Metabolism

111

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cachexia syndrome is a debilitating clinical condition characterizing the course of chronic diseases, which heavily impacts on patients' morbidity and quality of life, ultimately accelerating death. The pathogenesis is multifactorial and reflects the complexity and redundancy of the mechanisms controlling energy homeostasis under physiological conditions. Accumulating evidence indicates that, during disease, disturbances of the hypothalamic pathways controlling energy homeostasis occur, leading to profound metabolic changes in peripheral tissues. In particular, the hypothalamic melanocortin system does not respond appropriately to peripheral inputs, and its activity is diverted largely toward the promotion of catabolic stimuli (i.e., reduced energy intake, increased energy expenditure, possibly increased muscle proteolysis, and adipose tissue loss). Hypothalamic proinflammatory cytokines and serotonin, among other factors, are key in triggering hypothalamic resistance. These catabolic effects represent the central response to peripheral challenges (i.e., growing tumor, renal, cardiac failure, disrupted hepatic metabolism) that are likely sensed by the brain through the vagus nerve. Also, disease-induced changes in fatty acid oxidation within hypothalamic neurons may contribute to the dysfunction of the hypothalamic melanocortin system. Ultimately, sympathetic outflow mediates, at least in part, the metabolic changes in peripheral tissues. Other factors are likely involved in the pathogenesis of the anorexia-cachexia syndrome, and their role is currently being elucidated. However, available evidence shows that the constellation of symptoms characterizing this syndrome should be considered, at least in part, as different phenotypes of common neurochemical/metabolic alterations in the presence of a chronic inflammatory state. melanocortin; cytokines; serotonin; malonyl-coenzyme A; vagus nerve; sympathetic output THE ANOREXIA-CACHEXIA SYNDROME is a debilitating condition characterizing the clinical journey of patients suffering from chronic diseases including cancer, chronic obstructive pulmonary disease, tuberculosis, chronic heart failure, and end-stage renal insufficiency (64). As an experimental model, it represents a reliable and unique tool for the investigation of the mechanisms regulating energy intake and homeostasis. Beyond its relevance to human physiology, this syndrome impacts on clinical practice since it is highly prevalent and negatively influences patients' morbidity, mortality (66), and quality of life (57).The anorexia-cachexia syndrome is clinically characterized by a number of signs and symptoms interfering with energy intake (i.e., reduced appetite, early satiety, changes in taste/ smell) and affecting nutritional status (i.e., increased metabolic rate, weight loss, hormonal alterations, muscle and adipose tissue wasting, functional impairment, fatigue). At the biochemical and molecular levels, the main features of the anorexia-cachexia syndrome are the profound alterations of brain neurochemis...

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Involvement of plasma leptin, insulin and free tryptophan in cytokine-induced anorexia

Cited by 31 publications

References 43 publications

Time-Course Changes of Hormones and Cytokines by Lipopolysaccharide and Its Relation with Anorexia

Time-Course Changes of Hormones and Cytokines by Lipopolysaccharide and Its Relation with Anorexia

Leptin in immuno-rheumatological diseases

Neural control of the anorexia-cachexia syndrome

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