Description
The prevalence of type 2 diabetes is
significantly increased in the pediatric
population, which is affected by
obesity worldwide. The progression from
normal glucose tolerance (NGT) to type 2
diabetes involves intermediate stages of
impaired fasting glucose (IFG) and impaired
glucose tolerance (IGT), also
known as prediabetes. The pathophysiology
underlying the development of these
glucose metabolic alterations is multifactorial;
however an alteration in the balance
between insulin sensitivity and
insulin secretion represents the most important
player in the development of type
2 diabetes. Obese children and adolescents
affected by IGT and type 2 diabetes
are characterized by severe insulin resistance,
which is associated with an increased
lipid accumulation in visceral
compartments, liver and muscle tissues
and by reduced sensitivity of b-cell of first
and second-phase insulin secretion.
The progression in obese children of
insulin resistance to type 2 diabetes has
been shown to be faster than in adults; in
addition, type 2 diabetes is already associated
with several metabolic and cardiovascular
complications in this age group.
In the present review, we summarize
the most recent findings concerning the
prevalence of type 2 diabetes in youth and
in particular we explore the pathophysiology
of type 2 diabetes and the natural
history of this pathology in obese children
and adolescents.
Concurrent with the worldwide epidemic
increase of childhood obesity, type 2
diabetes and the two prediabetic conditions,
IFG and IGT, are becoming increasingly
more common in obese children and adolescents
(1,2). Until 10 years ago, type 2
diabetes accounted for less than 3% of all
cases of new-onset diabetes in adolescents.
At present 45% of cases are attributed to it
(3,4).
Type 2 diabetes occurs in youth more
often during the second decade of life,
coinciding with the physiological occurrence
of pubertal insulin resistance (1). In
addition,most children who develop type
2 diabetes (.75%of cases) have a first- or
second-degree relative affected by this pathology
(1).
The pathogenesis of type 2 diabetes is
complex, involving the interaction of
genetic and environmental risk factors
that strongly contribute to the development
of insulin resistance in the muscle
and liver as well as to b-cell failure, the
two core pathophysiological defects in
type 2 diabetes (5).