Sodium-coupled monocarboxylate transporters in normal tissues and in cancer.
Level 5 - mechanism / opinion, no new human data
Narrative review summarizing preclinical and mechanistic findings on monocarboxylate transporters without new clinical data.
PubMed 18446519 · doi:10.1208/s12248-008-9022-y
What was done
This paper reviews the expression, physiological roles, tumor-suppressive functions, and pharmacological substrate/inhibitor profiles of the sodium-coupled monocarboxylate transporters SLC5A8 and SLC5A12 based on published preclinical literature.
What was found
The abstract reports qualitative mechanistic descriptions without quantitative metrics or statistical numbers. SLC5A8 is a high-affinity transporter localized to apical membranes in the intestine and proximal tubule, as well as neurons and retinal pigment epithelium, transporting short-chain fatty acids, lactate, pyruvate, ketone bodies, and nicotinate. SLC5A12 is a low-affinity transporter expressed in intestinal and proximal tubule apical membranes, astrocytes, and Müller cells. SLC5A8 acts as a tumor suppressor silenced in colon, thyroid, stomach, kidney, and brain tumors through uptake of histone deacetylase inhibitors (butyrate, propionate, pyruvate). It also transports salicylates, benzoate, and gamma-hydroxybutyrate, and is blocked by NSAIDs (ibuprofen, ketoprofen, fenoprofen).
Why it matters
Characterizing SMCT transport mechanisms and tissue distribution clarifies how these proteins contribute to metabolic homeostasis, tumor suppression via epigenetic regulators, and potential drug interactions.
Limits
As a narrative review, no primary human dataset, statistical comparisons, or quantitative kinetic measurements are reported in the abstract. Evidence is based on preclinical mechanism-based models.
Cited by
- supports The intestinal lactate transporter belongs to a different gene family than the monocarboxylate transporters in cell membranes and functions as a sodium symport rather than a proton symport.