In addition to looking
at mouse models of diabetes, the researchers also showed that exposure of human pancreatic islet cells — both from healthy donors and from patients with Type 1 diabetes — to fasting - mimicking diet in a dish stimulated insulin production.
Not exact matches
Working in
mice that were put on high - fat diets to
model diabetes, «we demonstrated that obesity increases the expression
of pro-inflammatory genes in abdominal fat, but not in other organs such as the liver or muscle, nor in subcutaneous fat,» says Jongsoon Lee, PhD, Assistant Investigator in Joslin's Section on Pathophysiology and Molecular Pharmacology and Assistant Professor
of Medicine
at Harvard Medical School.
Tests on
mouse models for type 1
diabetes show that one injection works for a minimum
of 14 hours, during which time it can repeatedly and automatically lower blood sugar levels after
mice are given amounts
of sugar comparable to what they would consume
at mealtime.
The experimenters successfully tested the compound in the two
mouse models «either treating right
at the beginning
of diabetes, or for reversal
of toxic effects after three or four months
of diabetes, which is even more difficult,» King says.
After colleagues
at Sanofi provided an investigational compound that activates PKM2, the team showed that this compound could stop abnormalities in
mouse podocytes both in cell culture and in two
mouse models of diabetes.
Marc Claret, head
of the Neuronal Metabolism Control Group
at IDIBAPS, adds that «our results also suggest pathological implications
of this animal
model, since a diet rich in fats makes these
mice more susceptible to developing
diabetes.»