Gut Microorganisms and Autism: the Latest Research

LPS and Autism

LPS and Mercury

Treatments for LPS

LPS and Behavior

LPS and Detox

LPS and the Brain LPS and Thyroid LPS and GI System LPS and Immunity Other Effects of LPS
LPS and Inflammation LPS and Opioids LPS and Oxidative Stress LPS and Leaky Gut LPS and Candida
Anorexia and LPS NF-κB and LPS Mitochondria and LPS Liver and LPS Ammonia and LPS
Hypoglycemia and LPS Kidney and LPS Allergy and Bacteria Copper, Zinc and LPS Glutathione and LPS

Anorexia and LPS

Bacterial infections induce anorexia

LPS is a very common bacterial toxin. When mice are injected with LPS, they exhibit anorexia. Anorexia is a defense mechanism to fight bacterial infections. The more food an organism consumes, the more food there will be for the bacteria to flourish and increase. Temporary anorexia during disease may be beneficial to an organism since a restriction in food supply will inhibit bacterial growth.

Click here to view this article on PubMed

1: Am J Physiol. 1997 Jul;273(1 Pt 2):R181-6. LPS-induced anorexia in leptin-deficient (ob/ob) and leptin receptor-deficient (db/db) mice.

Faggioni R, Fuller J, Moser A, Feingold KR, Grunfeld C.

Department of Medicine, University of California, USA.

Administration of endotoxin (lipopolysaccharide, LPS) induces profound anorexia. Injection of leptin decreases food intake in mice. Recently, we reported that LPS and cytokines increase leptin levels in hamsters. To further investigate the role of leptin in the LPS-induced anorexia, we administered LPS to leptin receptor-deficient (db/db) and leptin-deficient (ob/ob) mice. We found that LPS caused anorexia in both db/db and ob/ob mice. As might be predicted if leptin had a role in anorexia, the db/db mice were somewhat resistant to LPS-induced anorexia. However the ob/ob mice were more sensitive to LPS-induced anorexia. No differences between db/db and ob/ob mice and their respective littermate were observed in circulating tumor necrosis factor levels after LPS. These data suggest that leptin per se is not essential for LPS-induced anorexia.

PMID: 9249548 [PubMed - indexed for MEDLINE]


Click here to view this article on PubMed

1: Neurosci Lett. 2003 May 29;343(1):25-8.Click here to read Links Bacterial lipopolysaccharide shifts fasted plasma ghrelin to postprandial levels in rats. Basa NR, Wang L, Arteaga JR, Heber D, Livingston EH, Taché Y.

CURE/Digestive Diseases Research Center, Digestive Diseases Division, David Geffen School of Medicine and Brain Research Institute, University of California at Los Angeles, Building 115, Room 203, 11301 Wilshire Boulevard, 90073, USA. nrbasa@ucla.edu

Lipopolysaccharide (LPS) injected intraperitoneally (i.p.) is known to decrease food intake. Ghrelin is a peptide hormone produced by the stomach with a potent orexigenic effect and plasma levels that are inversely correlated with the fed state. We examined changes in plasma ghrelin levels 3 h after LPS (100 microg/kg, i.p.) in fasted rats with or without a 1 h re-feeding period. LPS injection decreased the fasting levels of ghrelin by 51+/-5% compared with preinjection values while i.p. vehicle did not modify ghrelin levels in fasted rats. LPS at this dose reduced fasting-induced food intake by 60% compared with the i.p. vehicle group. Re-feeding decreased plasma ghrelin levels by 58+/-3% compared with pre-feeding fasting values in i.p. vehicle group. These data provide the first evidence that LPS shifts fasting ghrelin levels to those observed postprandially.

PMID: 12749989 [PubMed - indexed for MEDLINE]


Click here to view this article on PubMed

Nutrition. 1996 Feb;12(2):69-78.

Anorexia during acute and chronic disease.

Plata-Salamán CR.

Medical Sciences Faculty, School of Life and Health Sciences, University of Delaware, Newark 19716, USA.

Anorexia is associated with disorders of all systems. Anorexia represents a consistent clinical manifestation during acute and chronic pathophysiological processes (infection, inflammation, injury, toxins, immunological reactions, malignancy and necrosis). Anorexia during disease can be beneficial or deleterious depending on the timing and duration. Temporary anorexia during acute disease may be beneficial to an organism since a restriction in the intake of micro- and macro-nutrients will inhibit bacterial growth. Long-term anorexia during chronic disease, however, is deleterious to an organism and may be associated with cachexia, which can ultimately result in death. Various mechanisms participate in the anorexia observed during disease, including cytokine action. Anorexia induced by cytokines is proposed to involve modulation of hypothalamic-feeding associated sites, prostaglandin-dependent mechanisms, modifications of neurotransmitter systems, gastrointestinal, metabolic, and endocrine factors. In addition, the anorexia-cachexia syndrome is multifactorial and may involve chronic pain, depression or anxiety, hypogeusia and hyposmia, chronic nausea, early satiety, malfunction of the gastrointestinal system, metabolic alterations, cytokine action, production of other anorexigenic substances and/or iatrogenic causes (chemotherapy, radiotherapy). Cachexia may result not only from anorexia and a decreased caloric intake, but also from malabsorption and losses from the body (ulcers, hemorrhage, effusions), or a change in body metabolism. Research has focused on potential interventions to modify anorexia during disease and the anorexia-cachexia syndrome. Nutritional modifications and the use of specific steroids (such as megestrol acetate) are being tested in the clinical setting. Understanding the specific mechanisms responsible for anorexia during disease as well as their interactions is essential to develop interventions for the control of anorexia (during a critical time in a specific disease), and to devise less toxic immunotherapeutic regimens using cytokines.

PMID: 8724375 [PubMed - indexed for MEDLINE]