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

Kim, Yong-Woon; Kim, Keon-ho; Ahn, Dongbin; Kim, Hee-Sun; Kim, Jong-Yeon; Lee, Dong Chul; Park, So‐Young

doi:10.2170/physiolsci.rp003407

Cited by 44 publications

(27 citation statements)

References 52 publications

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“…3b. As was expected, the effect of single ip LPS administration on plasma levels of corticosterone 4 h after injection was less pronounced (4.56 fold), since it is well known that ip administration of LPS to rats and mice induces the elevation of plasma corticosterone reaching peak around 2 h [39]. Nevertheless, almost the same inhibitory effect of ip LPS ?…”

Section: Effect Of Lps Administration Alone or In Combination With Hesupporting

confidence: 60%

“…Many of the physiological effects associated with LPS are mediated by cytokines, including TNFa, IL-1 and IL-6, the levels of all being elevated as a result of LPS administration [38][39][40][41]. LPS administration activates HPA axis by increasing circulating concentration of adrenocorticotropic hormone (ACTH), which in turn induces downstream release of glucocorticoids from the adrenal cortex [38][39][40][41].…”

Section: Introductionmentioning

confidence: 99%

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Hemorphins Act as Homeostatic Agents in Response to Endotoxin-Induced Stress

et al. 2009

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The effect of synthetic LVV-hemorphin-7 and hemorphin-7 on hypothalamo-pituitary-adrenocortical axis activity in response to endotoxin-induced stress was studied. The intraperitoneal (ip) endotoxin (lipopolysaccaride, LPS) (0.5 mg/kg) administration in combination with hemorphin (1 mg/kg) induce significant decrease in plasma corticosterone and modest decrease in plasma levels of tumor necrosis factor-alpha (TNFalpha) in compare with elevated levels of both corticosterone and TNFalpha in plasma of rats received LPS administration alone. Increased activity of calcineurin in both plasma and brain of rats received ip administration of LPS, was recovered under LPS + hemorphin treatment. In two independent proteome analysis, using 2-dimensional fluorescence difference gel electrophoresis and the isotope coded protein label technology, peptidyl-prolyl cis-trans-isomerase A (cyclophilin A) was identified as regulated by hemorphins protein in mouse brain. A therapeutic potential of hemorphins and mechanisms of their homeostatic action in response to endotoxin-induced stress are discussed.

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Section: Effect Of Lps Administration Alone or In Combination With Hesupporting

confidence: 60%

Section: Introductionmentioning

confidence: 99%

Hemorphins Act as Homeostatic Agents in Response to Endotoxin-Induced Stress

et al. 2009

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“…1), corresponding to the observed decrease in food-intake [15,83,84]. More importantly, administration of NPY or blocking the induced inflammatory response in these animal models prevents the development of anorexia [15,85]. These data suggest that NPY release is necessary to adapt food intake to changes in energy expenditure.…”

Section: Hypothalamic Inflammation: Orexigenic Signallingmentioning

confidence: 79%

Hypothalamic inflammation and food intake regulation during chronic illness

et al. 2016

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“…In our study, single or repeated LPS induced no changes in p-ERK expression in either the mediobasal hypothalamus extracts or in the parvocellular portion of the PVN. p-ERK can be induced in the parvocellular corticotropinreleasing factor (CRF)-expressing neurons in the PVN in response to insulin (22), whose levels may increase after infectious stimuli such as LPS (24,42,54). We have previously reported that a single LPS injection increased CRF mRNA and Fos-CRF expression in the parvocellular PVN (5,41).…”

Section: E45 Leptin Resistance Induced By Long-term Exposure To Lpsmentioning

confidence: 99%

Protein tyrosine phosphatase-1B contributes to LPS-induced leptin resistance in male rats

Borges

Rorato

Uchôa

et al. 2015

American Journal of Physiology-Endocrinology and Metabolism

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Borges BC, Rorato RC, Uchoa ET, Marangon PB, Elias CF, Antunes-Rodrigues J, Elias LL. Protein tyrosine phosphatase-1B contributes to LPS-induced leptin resistance in male rats. Am J Physiol Endocrinol Metab 308: E40 -E50, 2015. First published October 28, 2014 doi:10.1152/ajpendo.00094.2014.-Leptin resistance is induced by the feedback inhibitors tyrosine phosphatase-1B (PTP1B) and decreased Src homology 2 domain-containing tyrosine phosphatase-2 (SHP-2) signaling. To investigate the participation of PTP1B and SHP-2 in LPS-induced leptin resistance, we injected repeated (6-LPS) intraperitoneal LPS doses (100 g/kg ip) for comparison with a single (1-LPS) treatment and evaluated the expression of SHP-2, PTP1B, p-ERK1/2, and p-STAT3 in the hypothalamus of male Wistar rats. The single LPS treatment increased the expression of p-STAT3 and PTP1B but not SHP-2. The repeated LPS treatment reduced SHP-2, increased PTP1B, and did not change p-STAT3. We observed that the PTP1B expression induced by the endotoxin was highly colocalized with leptin receptor cells in the hypothalamus of LepRb-IRESCre-tdTomato reporter mice. The single, but not the repeated, LPS treatment decreased the food intake and body weight. Leptin had no stimulatory effect on the hypophagia, body weight loss, or pSTAT3 expression in 6-LPS rats, indicating leptin unresponsiveness. Notably, the PTP1B inhibitor (3.0 nmol/rat in 5 l icv) restored the LPSinduced hypophagia in 6-LPS rats and restored the ability of leptin to reduce food intake and body weight as well as to phosphorylate STAT3 in the arcuate, paraventricular, and ventromedial nuclei of the hypothalamus. The present data suggest that an increased PTP1B expression in the hypothalamus underlies the development of leptin resistance during repeated exposure to LPS. Our findings contribute to understanding the mechanisms involved in leptin resistance during low-grade inflammation as seen in obesity. leptin resistance; endotoxemia; protein tyrosine phosphatase-1B; Src homology 2 domain-containing tyrosine phosphatase-2; extracellular signal-regulated kinases INFLAMMATION HAS BEEN DEMONSTRATED to be a common underlying cause of many obesity-associated conditions, such as diabetes and atherosclerosis (13,30,37,48). Rodent models of the obesity induced by a fat-enriched diet show enhancement of inflammatory cytokine secretion (37) and increased hypothalamic inflammatory signaling (44). Changes in gut microbiota are crucial factors in the development of obesity. Cani et al. (9) reported that high-fat feeding in mice augments plasma lipopolysaccharide (LPS) from gram-negative bacteria at a concentration sufficient to increase body weight and inflammation. In rats, the inflammation triggered by LPS and the subsequent activation of Toll-like receptor 4 (TLR4) has a determinant role in the development of the obese phenotype in response to high-fat/high-calorie food intake (14). Interestingly, exogenous long-term LPS infusion (300 g·kg Ϫ1 ·day Ϫ1for 4 wk) in normal-diet-fed mice caused a metabolic response t...

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

Cited by 44 publications

References 52 publications

Hemorphins Act as Homeostatic Agents in Response to Endotoxin-Induced Stress

Hemorphins Act as Homeostatic Agents in Response to Endotoxin-Induced Stress

Hypothalamic inflammation and food intake regulation during chronic illness

Protein tyrosine phosphatase-1B contributes to LPS-induced leptin resistance in male rats

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