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Leptin and diabetic foot ulcers

Discussion in 'Diabetic Foot & Wound Management' started by NewsBot, Sep 19, 2012.

  1. NewsBot

    NewsBot The Admin that posts the news.

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    Expression of leptin and its long-form receptor in the marginal cutaneous tissues of diabetic foot ulcers.
    Cao Y, Gao F, Li CZ, Xue YM.
    Acta Diabetol. 2012 Sep 18.
     
  2. Admin2

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  3. Admin2

    Admin2 Administrator Staff Member

    Leptin

    Leptin (from Greek λεπτός leptos, "thin" or "light" or "small") is a protein hormone predominantly made by adipocytes (cells of adipose tissue). Its primary role is likely to regulate long-term energy balance.[6]

    As one of the major signals of energy status, leptin levels influence appetite, satiety, and motivated behaviors oriented towards the maintenance of energy reserves (e.g., feeding, foraging behaviors).

    The amount of circulating leptin correlates with the amount of energy reserves, mainly triglycerides stored in adipose tissue. High leptin levels are interpreted by the brain that energy reserves are high, whereas low leptin levels indicate that energy reserves are low, in the process adapting the organism to starvation through a variety of metabolic, endocrine, neurobiochemical, and behavioral changes.[7]

    Leptin is coded for by the LEP gene. Leptin receptors are expressed by a variety of brain and peripheral cell types. These include cell receptors in the arcuate and ventromedial nuclei, as well as other parts of the hypothalamus and dopaminergic neurons of the ventral tegmental area, consequently mediating feeding.[8][9]

    Although regulation of fat stores is deemed to be the primary function of leptin, it also plays a role in other physiological processes, as evidenced by its many sites of synthesis other than fat cells, and the many cell types beyond hypothalamic cells that have leptin receptors. Many of these additional functions are yet to be fully defined.[10][11][12][13][14][15]

    In obesity, a decreased sensitivity to leptin occurs (similar to insulin resistance in type 2 diabetes), resulting in an inability to detect satiety despite high energy stores and high levels of leptin.[16] A synonym for LEP is OB (for obese).[17]

    1. ^ a b c GRCh38: Ensembl release 89: ENSG00000174697 - Ensembl, May 2017
    2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000059201 - Ensembl, May 2017
    3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
    4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
    5. ^ Zhang F, Basinski MB, Beals JM, Briggs SL, Churgay LM, Clawson DK, et al. (May 1997). "Crystal structure of the obese protein leptin-E100". Nature. 387 (6629): 206–209. Bibcode:1997Natur.387..206Z. doi:10.1038/387206a0. PMID 9144295. S2CID 716518.
    6. ^ Al-Hussaniy HA, Alburghaif AH, Naji MA (2021). "Leptin hormone and its effectiveness in reproduction, metabolism, immunity, diabetes, hopes and ambitions". Journal of Medicine and Life. 14 (5): 600–605. doi:10.25122/jml-2021-0153. PMC 8742898. PMID 35027962.
    7. ^ Hebebrand J, Hildebrandt T, Schlögl H, Seitz J, Denecke S, Vieira D, et al. (October 2022). "The role of hypoleptinemia in the psychological and behavioral adaptation to starvation: Implications for anorexia nervosa". Neuroscience and Biobehavioral Reviews. 141: 104807. doi:10.1016/j.neubiorev.2022.104807. PMID 35931221. S2CID 251259742.
    8. ^ Brennan AM, Mantzoros CS (June 2006). "Drug Insight: the role of leptin in human physiology and pathophysiology--emerging clinical applications". Nature Clinical Practice. Endocrinology & Metabolism. 2 (6): 318–327. doi:10.1038/ncpendmet0196. PMID 16932309. S2CID 13118779.
    9. ^ Bouret S, Levin BE, Ozanne SE (January 2015). "Gene-environment interactions controlling energy and glucose homeostasis and the developmental origins of obesity". Physiological Reviews. 95 (1): 47–82. doi:10.1152/physrev.00007.2014. PMC 4281588. PMID 25540138.
    10. ^ Cite error: The named reference pmid7624777 was invoked but never defined (see the help page).
    11. ^ Cite error: The named reference pmid7624778 was invoked but never defined (see the help page).
    12. ^ Cite error: The named reference pmid7624776 was invoked but never defined (see the help page).
    13. ^ Cite error: The named reference pmid7584987 was invoked but never defined (see the help page).
    14. ^ Considine RV, Considine EL, Williams CJ, Nyce MR, Magosin SA, Bauer TL, et al. (June 1995). "Evidence against either a premature stop codon or the absence of obese gene mRNA in human obesity". The Journal of Clinical Investigation. 95 (6): 2986–2988. doi:10.1172/JCI118007. PMC 295988. PMID 7769141.
    15. ^ Considine RV, Sinha MK, Heiman ML, Kriauciunas A, Stephens TW, Nyce MR, et al. (February 1996). "Serum immunoreactive-leptin concentrations in normal-weight and obese humans". The New England Journal of Medicine. 334 (5): 292–295. doi:10.1056/NEJM199602013340503. PMID 8532024.
    16. ^ Pan H, Guo J, Su Z (May 2014). "Advances in understanding the interrelations between leptin resistance and obesity". Physiology & Behavior. 130: 157–169. doi:10.1016/j.physbeh.2014.04.003. PMID 24726399. S2CID 12502104.
    17. ^ "LEP - Leptin precursor - Homo sapiens (Human) - LEP gene & protein". www.uniprot.org. Retrieved 8 May 2022.
     
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