Table 1.

Overview of main GLUTs in the liver, muscle, and adipose tissue and their tissue-specific function in metabolism

Tissue	Isoform	Tissue-specific function in metabolism
Liver	GLUT1	Postnatal development and organogenesis of the liver [89]; main glucose transporter in non-parenchymal cells, relatively low levels in hepatocytes [221]; elevated in non-alcoholic steatohepatitis (NASH), alcoholic liver disease (ALD) [109], and hepatocellular carcinoma (HCC) [267]; reduced surface expression in hepatitis C virus (HCV) infection [111]; may contribute to glucotoxicity and oxidative stress [220]
	GLUT2	Most abundant GLUT isoform in hepatocytes, responsible for bulk of glucose uptake, but does not directly mediate hepatic glucose output [80]; involved as hepatoportal glucose sensor [20, 21]; SLC2A2 deficiency causal for Fanconi–Bickel syndrome (FBS) [61, 144]; gene variants have been associated with fasting hyperglycemia, transition to type 2 diabetes, hypercholesterolemia, and the risk of cardiovascular diseases [60]; downregulated in HCV infection [111]
	GLUT5	Fructose transport, dietary fructose consumption associated with increased expression, non-alcoholic fatty liver disease (NAFLD) [10]
	GLUT8	Mediates fructose-induced de novo lipogenesis [44]; overexpression linked to decreased PPARγ expression levels [43]; expression correlates with circulating insulin in diabetic mice [77]; involved in trehalose-induced autophagy [150]
	GLUT9	High-capacity uric acid (UA) transporter; hepatic inactivation of the gene in adult mice leads to severe hyperuricemia and hyperuricosuria [177]
Muscle	GLUT1	Contributes to basal glucose transport and fiber type–specific expression [106, 146]; increased surface expression in metabolic stress [195, 216]; increased overload-induced muscle glucose uptake or hypertrophic growth [153]
	GLUT4	Most abundant GLUT isoform, responsible for bulk of insulin- and contraction-stimulated glucose uptake [50, 131, 148]; insulin/contraction-regulated subcellular distribution between intracellular compartments and cell surface [38, 58, 67, 229]; knockout mice display systemic insulin resistance and a mild diabetic phenotype [115]; overexpression improves insulin sensitivity [19, 237]; upregulated in response to exercise [185]; abundance in diabetic skeletal muscle is mostly unchanged [174]
	GLUT10	Localized in mitochondria, involved in mitochondrial dehydroascorbic acid (DHA) transport, may protect from oxidative stress [126]; increased in overload-induced muscle glucose uptake or hypertrophic growth [153]
	GLUT12	May act as insulin-responsive glucose transporter similar to GLUT4 [225]; upregulated in humans after intensive exercise training [224]
Adipose	GLUT1	Contributes to basal glucose transport, undergoes recycling through internal membrane compartments [94]; abundance unaffected in type 2 diabetes [105]
	GLUT8	Expression increases markedly during fat cell differentiation [206]; recycles between endosomal compartments and cell surface, mostly intracellular, in mature adipocytes unresponsive to insulin [9, 128]
	GLUT4	Most abundant GLUT isoform, responsible for bulk of insulin stimulated glucose uptake [104]; activity associated with activation of nuclear transcription factor carbohydrate-response element-binding protein (ChREBP), enhanced lipogenesis and production of branched fatty acid esters of hydroxy fatty acids (FAHFAs) and secretion of retinol binding protein 4 (RBP4) [91, 160, 261]; reduced abundance in type 2 diabetes [69, 219]
	GLUT10	Mitochondrial DHA transport, may protect from oxidative stress [126]