Evidence that tumor necrosis factor-alpha[ndash ]induced hyperinsulinemia prevents decreases of circulating leptin during fasting in rats☆
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Invited review: Mechanisms of hypophagia during disease
2021, Journal of Dairy ScienceCitation Excerpt :This group went on to show that the TNF receptor is required in adipose tissue for TNF-α-stimulated leptin responses (Finck and Johnson, 2000). Additionally, this TNF-α-mediated leptin secretion may be partially mediated by insulin (Medina et al., 2002), although the effects of insulin on leptin secretion can continue when TNF receptors are blocked (Finck and Johnson, 2000). Although an important role of leptin is to provide negative feedback on FI, there is evidence that it may potentiate the actions of cytokines to further reduce FI during illness (Figure 1).
Green tea polyphenol epigallocatechin-3-gallate suppresses toll-like receptor 4 expression via up-regulation of E3 ubiquitin-protein ligase RNF216
2017, Journal of Biological ChemistryCitation Excerpt :Also, macrophage-derived TNFα is known to induce hyperinsulinemia and induction of macrophage infiltration followed by MCP-1 expression, which is involved in a feedback loop resulting in additional TNFα production (8). TNFα also causes hyperinsulinemia (22). A recent clinical study demonstrated a significant correlation between serum TNFα levels and states of hyperinsulinemia (23).
Immunomodulatory actions of central ghrelin in diet-induced energy imbalance
2012, Brain, Behavior, and ImmunityCitation Excerpt :However, our finding that leptin levels were markedly increased in food-restricted animals seems unexpected in light of the previous results showing a compensatory decline of this anorexigenic hormone in rodents as a consequence of fasting (Ahrén et al., 1997; Kowalska et al., 1999; Medina et al., 2002; Kmiec et al., 2005). The apparent discrepancy might be due to the fact that food restriction in our study was rather long (30 days) and the resulting metabolic alterations were therefore presumably distinct from those observed during short-term fasting (Ahrén et al., 1997; Kowalska et al., 1999; Medina et al., 2002; Kmiec et al., 2005). Alternatively, the unexpected starvation-mediated upregulation of leptin could be secondary to the induction of inflammation, as proinflammatory cytokines such as TNF and IL-1 can increase expression of leptin mRNA in adipose tissue and circulating levels of leptin in rodents (Grunfeld et al., 1996; Faggioni et al., 1998).
Regulation of food intake: A clinical perspective
2005, Endocrinologia y NutricionPinealectomy Alters Adipose Tissue Adaptability to Fasting in Rats
2004, Metabolism: Clinical and ExperimentalLeptin, Ghrelin, and Proinflammatory Cytokines: Compounds with Nutritional Impact in Chronic Kidney Disease?
2003, Advances in Renal Replacement Therapy
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Supported by National Institutes of Health (NIH) Grants No. DK 50129 and DK 35747, the Juvenile Diabetes Association, the American Diabetes Association, the US Department of Agriculture, and the California Breast Cancer Research Program of the University of California, 1RB-0404. E.A.M. was supported by an Individual National Research Service Award (DK09950) from the NIH.