The db/db mouse model develop hyperphagic obesity and
nonketotic diabetes similar to non-insulin-dependent diabetes
mellitus in humans. Diabetic features in db/db mice
follow an age-dependent progression, with early insulin
resistance followed by an insulin secretory defect resulting
in profound hyperglycemia. Thus, db/db mouse model
has provided a useful resource to understand and treat thetype 2 diabetic condition. For these reasons, in the present
study, diabetic db/db mice were using as diabetes model.
The present results demonstrate that curcumin treatment
significantly decreased body weight in db/db mice.
It was reported that curcumin decreases body weight by
reducing body fat and increasing lean mass in both
high-fat-diet-induced obese and ob/ob mice [20].
Using mitochondria isolated from untreated db/db
mice, we demonstrated that hyperglycaemia increases mitochondrial
oxygen consumption in the liver and kidneys,
compared with non-diabetic wild type mice (Figure 2). This
finding contrasts with previous observation of mitochondrial
dysfunction in liver from these same mice, which was
characterized by a reduced respiratory capacity [21]. However,
another study, db/db hearts exhibited reduced cardiac
function and increased myocardial oxygen consumption;
whereas mitochondrial ROS generation and lipid and
protein peroxidation products were increased [22].
Thus, heart mitochondria from db/db mice exhibited
fatty acid–induced mitochondrial uncoupling and increased
expression of fatty acid oxidation genes and electron transfer
flavoproteins, whereas the content of the F1 α-subunit
of ATP synthase was reduced.