We are analyzing https://link.springer.com/article/10.1007/s13539-010-0015-1.

Title:
Pathophysiology and treatment of inflammatory anorexia in chronic disease | Journal of Cachexia, Sarcopenia and Muscle
Description:
Decreased appetite and involuntary weight loss are common occurrences in chronic disease and have a negative impact on both quality of life and eventual mortality. Weight loss in chronic disease comes from both fat and lean mass, and is known as cachexia. Both alterations in appetite and body weight loss occur in a wide variety of diseases, including cancer, heart failure, renal failure, chronic obstructive pulmonary disease and HIV. An increase in circulating inflammatory cytokines has been implicated as a uniting pathogenic mechanism of cachexia and associated anorexia. One of the targets of inflammatory mediators is the central nervous system, and in particular feeding centers in the hypothalamus located in the ventral diencephalon. Current research has begun to elucidate the mechanisms by which inflammation reaches the hypothalamus, and the neural substrates underlying inflammatory anorexia. Research into these neural mechanisms has suggested new therapeutic possibilities, which have produced promising results in preclinical and clinical trials. This review will discuss inflammatory signaling in the hypothalamus that mediates anorexia, and the opportunities for therapeutic intervention that these mechanisms present.
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Keywords {🔍}

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Topics {✒️}

alpha-melanocyte stimulating hormone stress-related neuroendocrine circuitry tumor necrosis factor-alpha cells/leukemia inhibitory factor nuclear factor-kappab activation plata-salamán cr article download pdf small-cell lung cancer lipopolysaccharide-induced anorexia depends body-cell-mass depletion agouti-related protein immunoreactivity blood-cerebrospinal fluid barrier intramedullary prostaglandin-dependent mechanism tumor-bearing animals show post-injection food intake tumor-bearing animals resulted anorectic tumor-bearing rats stimulating agrp/npy neurons wild-type anorexic mice agouti-related peptide/neuropeptide murine blood-brain barrier il-1 beta-induced anorexia c-fos mrna induced il-1β-induced anorexia left ventricular dysfunction leukemia inhibitory factor open access license tumor necrosis factor improve food intake skeletal muscle hypertrophy peripheral anti-catabolic effects attenuate cytokine-induced anorexia agouti-related protein normal body-weight homeostasis privacy choices/manage cookies reduce cancer-induced cachexia il-1β mrna expression hypothalamic agrp/npy neurons orexigenic agrp/npy neurons leukaemia inhibitory factor banks wa pro-opiomelanocortin processing npy-induced feeding response improves food intake bioactive products including cancer-related anorexia/cachexia murine il-1 alpha ameliorates anorexia induced peripheral interleukin-1beta administration tumor-bearing mice [90

Questions {❓}

Differential leptin access into the brain–a hierarchical organization of hypothalamic leptin target sites?
Y eat?

Schema {🗺️}

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         headline:Pathophysiology and treatment of inflammatory anorexia in chronic disease
         description:Decreased appetite and involuntary weight loss are common occurrences in chronic disease and have a negative impact on both quality of life and eventual mortality. Weight loss in chronic disease comes from both fat and lean mass, and is known as cachexia. Both alterations in appetite and body weight loss occur in a wide variety of diseases, including cancer, heart failure, renal failure, chronic obstructive pulmonary disease and HIV. An increase in circulating inflammatory cytokines has been implicated as a uniting pathogenic mechanism of cachexia and associated anorexia. One of the targets of inflammatory mediators is the central nervous system, and in particular feeding centers in the hypothalamus located in the ventral diencephalon. Current research has begun to elucidate the mechanisms by which inflammation reaches the hypothalamus, and the neural substrates underlying inflammatory anorexia. Research into these neural mechanisms has suggested new therapeutic possibilities, which have produced promising results in preclinical and clinical trials. This review will discuss inflammatory signaling in the hypothalamus that mediates anorexia, and the opportunities for therapeutic intervention that these mechanisms present.
         datePublished:2010-12-17T00:00:00Z
         dateModified:2010-12-17T00:00:00Z
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      headline:Pathophysiology and treatment of inflammatory anorexia in chronic disease
      description:Decreased appetite and involuntary weight loss are common occurrences in chronic disease and have a negative impact on both quality of life and eventual mortality. Weight loss in chronic disease comes from both fat and lean mass, and is known as cachexia. Both alterations in appetite and body weight loss occur in a wide variety of diseases, including cancer, heart failure, renal failure, chronic obstructive pulmonary disease and HIV. An increase in circulating inflammatory cytokines has been implicated as a uniting pathogenic mechanism of cachexia and associated anorexia. One of the targets of inflammatory mediators is the central nervous system, and in particular feeding centers in the hypothalamus located in the ventral diencephalon. Current research has begun to elucidate the mechanisms by which inflammation reaches the hypothalamus, and the neural substrates underlying inflammatory anorexia. Research into these neural mechanisms has suggested new therapeutic possibilities, which have produced promising results in preclinical and clinical trials. This review will discuss inflammatory signaling in the hypothalamus that mediates anorexia, and the opportunities for therapeutic intervention that these mechanisms present.
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         Pharmacology/Toxicology
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