
Type 2 diabetes (T2D) is one of the major and exacer-
bating health problems worldwide; T2D is predicted to
affect 490 million in 2030 (Zhang, et al., 2010). Strong
genetic in uences and many polymorphisms have been
reproducibly associated with T2D.Insulin resistance in
muscle, liver, and adipose tissues is a primary charac-
teristic of most patients with T2D; as such, these tissues
become resistant to endogenous and exogenous insulin.
The interaction of insulin with target tissues is mediated
by insulin receptor (INSR), a glycoprotein implicated
in directing insulin to target cells and initiating cell
responses to insulin, (Gold ne, 1987 Herder and Roden,
2011, Voight, et al., 2010).
High-mobility group A1 (HMGA1) is an architectural
transcription factor involved in numerous biological
functions in the nucleus, including regulation of DNA
replication, transcription, recombination, and repair;
among these functions, transcriptional regulation of
gene expression is considered as the most important.
After HMGA1 binds to DNA, HMGA1 can be polymerized
with other transcription factors, forming an “enhanceo-
some†to regulate gene transcription; thus, gene expres-
sions are positively or negatively regulated(Bustin and
Reeves, 1996). Studies on humans and knockout mice
have suggested that HMGA1 is involved in to T2D patho-
genesis through the regulation of INSR gene expres-
sion; INSR gene expression is decreased by functional
HMGA1 gene variants. HMGA1-de cient patients have
been biologically investigated because of their clinical
value. However, whether HMGA1 single gene deletion-
or mutation-induced insulin resistance is the underlying
cause of T2D remains unknown, (Foti, et al., 2005). Low-
frequency insertion polymorphism IVS5-13insC (c.136-
14_136-13insC) has been identi ed and associated with
insulin resistance and T2D among individuals of white
European ancestry and Chinese populations, (Chiefari,
et al., 2011 Liu, et al., 2012)
Published:
2017-10-03