Table 3.
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 |