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. 2022 Feb 24;13:847611. doi: 10.3389/fendo.2022.847611

Table 3.

The roles of KYNA in metabolic diseases.

Organ/cell KYNA production Effects Associated metabolic disease
Liver High expression levels of TDO/IDO/KYATs were detected in liver (12) Activation of GPR35 inhibits the development of NAFLD (5) NAFLD
Inhibition of Kuffer cells NMDA receptor by KYNA limits inflammasome activation (76) Metabolic inflammation
Activation of AMPK/autophagy‐ and AMPK/ORP150 pathway by KYNA ameliorate endoplasmic reticulum stress and hepatic steatosis (6) Hepatic steatosis
Adipose tissue/adipocyte Expression of IDO1/KYAT1/KYAT3 were detected in adipocytes (3) Activation of GPR35 by KYNA promotes the expression of PGC1-α and UCP1 (67) Insulin resistance
Activation of GPR35/AMPK and SIRT6 pathways by KYNA reduces inflammation and insulin resistance in adipocytes (87) Metabolic inflammation
Muscle Endurance essences enhance KYATs expression and promote KYNA production (64, 65, 67) Activation of GPR35/AMPK and SIRT6 pathways by KYNA reduces inflammation and insulin resistance in skeletal muscle (87) Insulin resistance
Metabolic inflammation
Immune cell KYAT1/KYAT2 expressions were detected in in both unstimulated and stimulated macrophage (107) Antagonize NMDA receptor by KYNA inhibits ABCA1 degradation (75) Cholesterol accumulation
Activation of GPR35 by KYNA induces autophagy-dependent degradation of NLRP3 in macrophage (84) Metabolic inflammation
Pancreas KYNA were detected in pancreas fluid, expression of TDO/KYATs were detected in pancreatic islets (9, 13) High concentration of KYNA enhances glucose stimulated insulin secretion (13) Type 2 diabetes
Mammary gland KYNA content in breast milk gradually increases in different lactation periods (10) KYNA may act as an anti-obese agent for children (10) Obesity