Lactate was initially found to activate HCA1 on
fat cells and thereby to inhibit these cells
lipolysis i.e., break-down of their fats into
free fatty acids and
glycerol.[10][11] Subsequent studies have found that in addition to fat cells, HCA1 is expressed on cells in the brain, skeletal muscle, lymphoid tissue, uterus, kidney, liver, and pancreas as well as on immune cells such as
macrophages and
antigen-presenting cells. In the brain, HCA1 acts to dampen
neuron excitation and may also function to promote
neurogenesis (i.e., production of neurons from
neural stem cells) and
angiogenesis, i.e., formation of new blood vessels from pre-existing blood vessels). The functions of HCA1 in non-fat and non-neural tissues have not been fully defined but in many cases appear to involve promoting the survival of cells, including various types of cancer cells.[12]
^
abS Offermanns, SL Colletti, AP IJzerman, TW Lovenberg, G Semple, A Wise, MG Waters.
"Hydroxycarboxylic acid receptors". IUPHAR/BPS Guide to Pharmacology. International Union of Basic and Clinical Pharmacology. Retrieved 13 July 2018.{{
cite web}}: CS1 maint: multiple names: authors list (
link)
^Wagner W, Sobierajska K, Pułaski Ł, Stasiak A, Ciszewski WM (April 2023). "Whole grain metabolite 3,5-dihydroxybenzoic acid is a beneficial nutritional molecule with the feature of a double-edged sword in human health: a critical review and dietary considerations". Critical Reviews in Food Science and Nutrition: 1–19.
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10.1080/10408398.2023.2203762.
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^Cai TQ, Ren N, Jin L, Cheng K, Kash S, Chen R, Wright SD, Taggart AK, Waters MG (December 2008). "Role of GPR81 in lactate-mediated reduction of adipose lipolysis". Biochemical and Biophysical Research Communications. 377 (3): 987–91.
doi:
10.1016/j.bbrc.2008.10.088.
PMID18952058.
^Colucci AC, Tassinari ID, Loss ED, de Fraga LS (June 2023). "History and Function of the Lactate Receptor GPR81/HCAR1 in the Brain: A Putative Therapeutic Target for the Treatment of Cerebral Ischemia". Neuroscience. 526: 144–163.
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10.1016/j.neuroscience.2023.06.022.
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