R Di Paola1, A Marucci2, V Trischitta3. 1. Research Unit of Diabetes and Endocrine Diseases, IRCCS "Casa Sollievo della Sofferenza", San Giovanni Rotondo, Italy. Electronic address: r.dipaola@operapadrepio.it. 2. Research Unit of Diabetes and Endocrine Diseases, IRCCS "Casa Sollievo della Sofferenza", San Giovanni Rotondo, Italy. 3. Research Unit of Diabetes and Endocrine Diseases, IRCCS "Casa Sollievo della Sofferenza", San Giovanni Rotondo, Italy; Department of Experimental Medicine, Sapienza University, Rome, Italy. Electronic address: vincenzo.trischitta@operapadrepio.it.
Abstract
A wide range of studies both in humans and animal models point GALNT2 as a shaper of serum HDL-C and TG levels. Available data in humans indicate that, while under conditions of extreme GALNT2 loss-of-function HDL-C is the main target, a fine-tuning of GALNT2 changes is mostly associated with TG levels. Understanding whether different degrees of GALNT2 change do modulate different serum lipid fractions and, if so, addressing the mechanisms underlying such pleiotropic effects has the potential not only to improve our understanding of HDL-C and TG metabolism, but also to make GALNT2 becoming a target for treating atherogenic dyslipidemia and related clinical events.
A wide range of studies both in humans and animal models point GALNT2 as a shaper of serum HDL-C and TG levels. Available data in humans indicate that, while under conditions of extreme GALNT2 loss-of-function HDL-C is the main target, a fine-tuning of GALNT2 changes is mostly associated with TG levels. Understanding whether different degrees of GALNT2 change do modulate different serum lipid fractions and, if so, addressing the mechanisms underlying such pleiotropic effects has the potential not only to improve our understanding of HDL-C and TG metabolism, but also to make GALNT2 becoming a target for treating atherogenic dyslipidemia and related clinical events.