Scribd
Upload
51 views2 pages

Scribd

Insulin resistance has long been considered a key factor in type 2 diabetes, but recent reviews have questioned this. While insulin resistance is seen in type 2 diabetes, it is also seen in other conditions like obesity, hypertension, and heart disease. Some argue insulin resistance in type 2 diabetes is entirely due to obesity. Prospective studies show insulin deficiency or resistance can precede diabetes, but their relative contributions remain unclear. Both insulin resistance and deficiency contribute to established type 2 diabetes.

Uploaded by

Hannah Vuelta
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
51 views2 pages

Scribd

Insulin resistance has long been considered a key factor in type 2 diabetes, but recent reviews have questioned this. While insulin resistance is seen in type 2 diabetes, it is also seen in other conditions like obesity, hypertension, and heart disease. Some argue insulin resistance in type 2 diabetes is entirely due to obesity. Prospective studies show insulin deficiency or resistance can precede diabetes, but their relative contributions remain unclear. Both insulin resistance and deficiency contribute to established type 2 diabetes.

Uploaded by

Hannah Vuelta
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
You are on page 1/ 2

Insulin resistance

Emanating from the prismatic demonstration by Yalow and Berson of the presence of
hyperinsulinism in type 2 diabetes, insulin resistance has been considered to play an integral role
in the pathogenesis of the disease (36). Recent critical reviews, however, have questioned the
primacy, specificity, and contribution of insulin resistance to the disease state (37, 38). As
chronic hyperinsulinemia inhibits both insulin secretion (39) and action (40), and hyperglycemia
can impair both the insulin secretory response to glucose (41) as well as cellular insulin
sensitivity (42, 43), the precise relation between glucose and insulin level as a surrogate measure
of insulin resistance has been questioned. Lean type 2 diabetic patients over 65 yr of age have
been found to be as insulin sensitive as their age-matched nondiabetic controls (44). Moreover,
in the majority of type 2 diabetic patients who are insulin resistant, obesity is almost invariably
present (45, 46). As obesity or an increase in intraabdominal adipose tissue is associated with
insulin resistance in the absence of diabetes, it is believed by some that insulin resistance in type
2 diabetes is entirely due to the coexistence of increased adiposity (47). Additionally, insulin
resistance is found in hypertension, hyperlipidemia, and ischemic heart disease, entities
commonly found in association with diabetes (16, 48, 49), again raising the question as to
whether insulin resistance results from different pathogenetic disease processes or is unique to
the presence of type 2 diabetes (16, 50, 51).
Prospective studies have demonstrated the presence of either insulin deficiency or insulin
resistance before the onset of type 2 diabetes (48). Two studies have reported the presence of
insulin resistance in nondiabetic relatives of diabetic patients at a time when their glucose
tolerance was still normal (52, 53). In addition, first degree relatives of patients with type 2
diabetes have been found to have impaired insulin action upon skeletal muscle glycogen
synthesis due to both decreased stimulation of tyrosine kinase activity of the insulin receptor and
reduced glycogen synthase activity (54, 55). Other studies in this high risk group have failed to
demonstrate insulin resistance, and in the same group, impaired early phase insulin release and
loss of normal oscillatory pattern of insulin release have been described (56, 57). Based upon
these divergent studies, it is still impossible to dissociate insulin resistance from insulin
deficiency in the pathogenesis of type 2 diabetes. However, both entities unequivocally
contribute to the fully established disease.
The liver

You might also like