Key result
Chronic cold exposure reverses feeding-regulated scWAT LPL activity via the hepatic insulin-ANGPTL8-ANGPTL3 axis.
Chronic cold exposure reprograms feeding-regulated LPL activity in white adipose tissue via the hepatic insulin-ANGPTL8-ANGPTL3 axis, highlighting a mechanism for triglyceride metabolism during adipose browning.
Answers are grounded in this paper and cite their sources.
Cold-induced hepatic ANGPTL axis may reprogram murine lipid handling during browning; leaves open translation to human triglyceride metabolism or cardiometabolic risk.
Graphical Abstract Lipoprotein lipase (LPL) mediates peripheral tissue triglyceride (TG) uptake. Hepatic ANGPTL3 (A3) and ANGPTL8 (A8) form a complex and inhibit LPL activity in the white adipose tissue (WAT) via systematic circulation. ANGPTL4 (A4) is expressed in WAT and inhibits LPL activity locally. Feeding increases hepatic A8 expression and increases its inhibition for WAT LPL activity together with A3, while feeding suppresses WAT A4 expression and releases its inhibition on LPL. At room temperature, the feeding-suppressed A4 overrides the feeding-increased A3/A8, resulting in increased LPL activity in WAT by food intake. Browning improves hepatic insulin sensitivity and increases postprandial A8 expression. The feeding-increased A3/A8 overrides the feeding-suppressed A4, resulting in suppressed LPL activity in WAT by food intake. This reprogrammed LPL regulation plays an important role in reprogramming TG metabolism during adipose tissue browning.
No takes yet. Share an insight, caveat, or question.
Zhang et al. (2024) studied Adipose tissue browning (preclinical model). Chronic cold exposure vs. Room temperature was evaluated on Tissue lipoprotein lipase (LPL) activity. Chronic cold exposure reversed feeding-regulated LPL activity in subcutaneous white adipose tissue through the hepatic insulin-ANGPTL8-ANGPTL3 axis.
Synapse has enriched 10 related papers. Consider them for comparative context: