COL6A3 and Insulin resistance: Notably, this finding aligns with those of previous studies showing that the collagen matrix surrounding subcutaneous fat is rich in C-terminal COL6A3 (ref. 39), which in turn releases endotrophin; and that increased expression of COL6A3 in subcutaneous adipose tissues and increased plasma abundance of endotrophin, the cleaved product of the C-terminal of COL6A3, are associated with adipose tissue fibrosis, insulin resistance and metabolic dysfunction40,42–45.