Proton-coupled monocarboxylate transporter. Catalyzes the rapid transport across the plasma membrane of many monocarboxylates such as lactate, pyruvate, branched-chain oxo acids derived from leucine, valine and isoleucine, and the ketone bodies acetoacetate, beta-hydroxybutyrate and acetate. Depending on the tissue and on cicumstances, mediates the import or export of lactic acid and ketone bodies. Required for normal nutrient assimilation, increase of white adipose tissue and body weight gain when on a high-fat diet. Plays a role in cellular responses to a high-fat diet by modulating the cellular levels of lactate and pyruvate, small molecules that contribute to the regulation of central metabolic pathways and insulin secretion, with concomitant effects on plasma insulin levels and blood glucose homeostasis. Interacts with isoform 2 of BSG; interaction mediates SLC16A1 targeting to the plasma membrane (PubMed:21792931). Interacts with EMB; interaction mediates SLC16A1 targeting to the plasma membrane (By similarity). Detected in liver, brain, spinal cord, spermatozoa, muscle, white adipose tissue and brown adipose tissue (at protein level). Widely expressed, except in pancreas, where expression is not detectable. Complete lethality during early embryonic development. Heterozygous mice are viable and show no obvious morphological or behavorial phenotype. Heterozygous mice that are kept on a normal diet show normal weight gain, normal glucose tolerance and insulin sensitivity. In contrast, mice exhibit a striking reduction in weight gain relative to wild-type, when kept on a high-fat diet. This is due to reduced fat accumulation in the liver and in subcutaneous white adipose tissue. In addition, heterozygous mice kept on a high-fat diet show higher glucose tolerance and higher insulin sensitivity than wild-type. The reduced weight gain is explained by reduced food intake, less efficient nutrient assimilation in the intestine and increased oxygen consumption when kept on a high-fat diet. Besides, heterozygous mice fail to respond to a high-fat diet by up-regulation of genes involved in lipid metabolism. Overexpression in pancreatic beta-cells triggers insulin secretion in response to pyruvate, causing hyperinsulemia and hypoglycemia during strenuous exercise. Belongs to the major facilitator superfamily. Monocarboxylate porter (TC 2.A.1.13) family.