However, its association with insulin resistance and betacell function remains controversial.
2
Hence, our results implicate both CTL and cytokines in betacell destruction.
3
Insulin resistance and betacell function were assessed with the homeostasis model.
4
ATT also extended islet viability in mice after streptozotocin-induced betacell toxicity.
5
Objective: Study the role of hyperglycemia-induced betacell loss on grafted islet destruction.
1
The pancreaticbetacell is the major source of circulating insulin in adult mammals.
2
Glucocorticoid doses, insulin sensitivity and pancreaticbetacell function were compared among these groups.
3
In males, insulin resistance progresses to a severe form of diabetes accompanied by pancreaticbetacell failure.
4
APX-115 significantly improved pancreaticbetacell function by decreased fasting blood glucose levels and increased insulin levels.
5
These female SLE patients with hyperglycemia were characterized by insulin resistance and reduced pancreaticbetacell function, and they were relatively young.
Uso de β-cell en inglés
1
However, SFRP4 does not control glucose homeostasis and β-cell mass in mice.
2
The islet β-cell is unusual in that glucose lacks an extracellular receptor.
3
This effect was not associated with enhanced β-cell proliferation or mass.
4
Type 2 diabetes incidence increases with age, while β-cell replication declines.
5
This was paralleled by an increase in β-cell proliferation and mass.
6
Insulin sensitivity and β-cell function were examined by homeostasis model assessment.
7
Of these, 16 had not previously been implicated in the regulation of β-cell mass.
8
Monogenic diabetes is caused by mutations that reduce β-cell function.
9
CAG repeat length did not show any significant correlation with IR or β-cell function.
10
In this study, we show how this coupling can produce oscillations in β-cell activity.
11
Here we show that palmitate-induced β-cell apoptosis is mediated by the intrinsic mitochondrial pathway.
12
Thus, MKP-1 is a possible target for anti-inflammatory therapeutic intervention with preservation of β-cell function.
13
Hence, factors controlling functional β-cell compensation are potentially important targets for the treatment of T2D.
14
Glycemia and β-cell function were assessed 1 week later at the peak of viral expression.
15
These data indicate that short-term HFD feeding enhances β-cell proliferation before insulin resistance becomes apparent.
16
Ex-4 nearly normalized both human β-cell survival and rodent β-cell replication when co-administered with tacrolimus.