Diabetes is one of the five leading causes of death in the world, with type 2 diabetes occurring more frequently than type 1. Management of diabetes without side effects is still a challenge and therefore new strategies need to be examined. Because of difficulties in human research, animal models of diabetes are useful research tools for this purpose and rodent models of type 2 diabetes are the first choice. The aim of this study is an overview on one of the most frequently used models of type 2 diabetes in rat, induced by streptozotocin and nicotinamide, considering its advantages and disadvantages for diabetes research in humans.
BackgroundCoronary artery disease is 2-3 times more common in diabetic individuals.
Dietary nitrate/nitrite has beneficial effects in both diabetes and
cardiovascular disease. It also has protective effects against myocardial
ischemia-reperfusion (IR) injury in healthy animals. However, the effects of
nitrate on myocardial IR injury in diabetic rats have not yet been
investigated.ObjectiveWe examined the effects of dietary nitrate on myocardial IR injury in
streptozotocin-nicotinamide-induced diabetic rats.MethodRats were divided into four groups (n=7 in each group): control,
control+nitrate, diabetes, and diabetes+nitrate. Type 2 diabetes was induced
by injection of streptozotocin and nicotinamide. Nitrate (sodium nitrate)
was added to drinking water (100 mg/L) for 2 months. The hearts were
perfused in a Langendorff apparatus at 2 months and assessed before
(baseline) and after myocardial IR for the following parameters: left
ventricular developed pressure (LVDP), minimum and maximum rates of pressure
change in the left ventricle (±dP/dt), endothelial nitric oxide (NO)
synthase (eNOS) and inducible NO synthase (iNOS) mRNA expression, and levels
of malondialdehyde (MDA) and NO metabolites (NOx).ResultsRecovery of LVDP and ±dP/dt was lower in diabetic rats versus
controls, but almost normalized after nitrate intake. Diabetic rats had
lower eNOS and higher iNOS expression both at baseline and after IR, and
dietary nitrate restored these parameters to normal values after IR.
Compared with controls, heart NOx level was lower in diabetic rats at
baseline but was higher after IR. Diabetic rats had higher MDA levels both
at baseline and after IR, which along with heart NOx levels decreased
following nitrate intake.ConclusionDietary nitrate in diabetic rats provides cardioprotection against IR injury
by regulating eNOS and iNOS expression and inhibiting lipid peroxidation in
the heart.
Background and objective:
The effects of hypothyroidism during pregnancy and lactation on carbohydrate metabolism have been mostly studied in male animals. The aim of this study is therefore to investigate effect of fetal and neonatal hypothyroidism (FH and NH) on the glucose tolerance in middle-aged female rat offspring.
Methods:
Pregnant female rats were divided into three groups: Rats in the control group consumed tap water, while those in
the FH and NH groups consumed 250 mg/L of 6-propyl-2-thiouracil (PTU) in their drinking water during gestation or lactation periods, respectively. After weaning, the female offspring were separated and divided into 3 groups (n=8/group): Control, FH, and NH. Body weight was recorded monthly and intravenous glucose tolerance test (IVGTT) was performed at
month 12.
Results:
Compared to controls, female rats in the FH group had significantly higher plasma glucose levels than controls
throughout the IVGTT except at min 60. Values at min 5 of the FH and control group were 196.1±1.9 and 155.3±5.9 mg/dL,
respectively (P<0.05). In the NH group, plasma glucose levels were significantly higher only at min 5 (185.7±14.1 vs.
155.3±5.9 mg/dL, P<0.05).
Conclusion:
Hypothyroidism during fetal or neonatal periods caused glucose intolerance in middle-aged female offspring
rats.
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