Table 2.

Animal model phenotypes relative to representative Slc transporters.

Slc	Diseases/defects	Animal models	References
Slc2a4	Fasting hyperglycemia and glucose intolerance	Global Slc2a4-deficient mice	Katz et al. (1995)
Slc2a4	Glucose uptake reduced by 75%	Muscle-specific Glut4 knockout (KO) mice	Zisman et al. (2000)
Slc2a4	Insulin resistance secondarily in muscle and liver	Adipose-specific Glut4 KO mice	Yang et al. (2005)
Slc2a4	Impaired ability in mouse under stress	Cardiac-specific Glut4 KO mice	Wende et al. (2017)
Slc2a4	Protection from albuminuria and diabetic nephropathy	Podocyte-specific Glut4 KO mice	Guzman et al. (2014)
Slc2a9	Hyperuricaemia, hyperuricosuria, spontaneous hypertension, dyslipidemia, and elevated body fat	Glut9 KO mice	DeBosch et al. (2014)
Slc3a1	Cystinuria	Slc3a1 KO Feline	Mizukami et al. (2015)
Slc5a2	Prevention from HFD-induced hyperglycemia and glucose intolerance; reduced plasma insulin concentrations	Slc5a2 KO mice	Jurczak et al. (2011)
Slc6a15	Less anxiety- and depressive-like behavior	Slc6a15 KO mice	Santarelli et al. (2016)
Slc6a15	Increased anxiety-like behavior	Slc6a15 overexpression mice	Santarelli et al. (2016)
Slc11a1	Sensitive to Salmonella typhimurium infection	Slc11a1 KO mice	Caron et al. (2006)
Slc12a1	Decreased neuronal layer thickness and cell number; more immature interneurons	Slc12a1 KO mice	Haering et al. (2015); Magalhaes and Rivera (2016)
Slc13a1	Hyposulfatemia	NaS1-null (Nas1−/−) mice	Markovich (2012b)
Slc15a1	Higher plasma amino acid levels	Slc15a1 KO mice	Yang et al. (2013)
Slc15a2	Lower body weight and lower relative heart weight in male PEPT2-null mice; lower relative kidney weight in female mice	PEPT2-null mice	Frey et al. (2006)
Slc16a1	Hyperinsulinism	RIP7-rtTA/Mct1-Luc mice	Pullen et al. (2012)
Slc17a1	Normal plasma Pi and calcium levels; reduced Pi excretion	NPT1−/− mice	Miyamoto et al. (2011)
Slc19a3	Neurodegenerative disorder	Slc19a3-deficient mice	Suzuki et al. (2017)
Slc20a2	Dysregulated phosphate homeostasis basal ganglia calcification	Heterzygous (Het) Slc20a2 mice	Jensen et al. (2013)
Slc23a1	Lower plasma ascorbate concentrations; brain hemorrhage	Slc23a1 KO mice	Sotiriou et al. (2002)
Slc24a4	A deficit in olfactory neurons	Slc24a4 KO mice	Li and Lytton (2014)
Slc26a1	Hyposulfatemia, hyperoxalemia; transport anions including sulfate, bicarbonate, chloride, and oxalate	Sat1-null (Sat1−/−)/Sat1 KO mice	Markovich (2012a)
Slc27a1	Reduced insulin resistance; decreased electroretinogram response	Slc27a1 KO mice	Kim et al. (2004); Chekroud et al. (2012)
Slc30a8	Islets with markedly fewer dense cores but more rod-like crystals	ZnT8-null (Slc30a8−/−) mice	Nicolson et al. (2009)
Slc38a3	Stunted growth, altered amino acid levels, hypoglycemia, and 20-day life; higher glutamine but reduced glutamate and γ-aminobutyric acid (GABA) levels in brain; reduced renal ammonium excretion	Snat3 mutant mice; Snat3-deficient mice	Chan et al. (2016)
Slc39a14	Impairs hepatic Mn uptake and biliary excretion, resulting in the accumulation of Mn in the circulation and brain	Global Slc39a14 KO mice; hepatocyte-specific Slc39a14 KO mice	Xin et al. (2017)

Slc functions were identified in genetically modified animal models. Slc deficiency has the potential to cause direct metabolic disorders or increase the susceptibility to diseases.