Key result
Spontaneously hypertensive rats had significantly higher insulin levels and lower glucose uptake by heart and striated muscle compared to controls, whereas secondary hypertension models did not.
Why the study?
Is insulin resistance a primary defect or secondary phenomenon in different rat models of hypertension?
Is insulin resistance a primary defect or secondary phenomenon in different rat models of hypertension?
Insulin resistance is a primary defect in spontaneously hypertensive rats, rather than a secondary consequence of hypertension, as it is absent in secondary hypertension models.
No takes yet. Share an insight, caveat, or question.
Insulin resistance may be primary in genetic hypertension; leaves open causality in human essential hypertension.
Bursztyn et al. (1992) studied Hypertension. Spontaneous hypertension (SHR model) vs. Secondary hypertension models (DOCA-salt, RVH) and normotensive controls was evaluated on Glucose metabolism (plasma half-life and tissue uptake of 3H-DOG, insulin levels). Spontaneously hypertensive rats had significantly higher insulin levels and lower glucose uptake by heart and striated muscle compared to controls, whereas secondary hypertension models did not.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: