Objective Maternal obesity pre-programmes offspring to develop obesity, glucose intolerance and associated cardiovascular disease later in life although the underlying mechanism is currently unknown. This study investigated the effect of a maternal high fat diet on perivascular adipose tissue (PVAT) regulation of resistance artery tone.
Design and method 8 week old female SD rats were fed a 10% fat diet (controls) or 45% fat obesogenic diet (HFD) for 12 weeks before mating then continued on their respective diets during pregnancy and lactation. PVAT-intact or -denuded mesenteric arteries from dams and pups (250–300 µm internal diameter) were mounted on a wire myograph. Cumulative concentration-response curves were constructed to thromboxane A2 receptor agonist U46619 (10 nM–3 µM) ± 10 µM A769662, an activator of AMP-activated kinase (AMPK), and/or 100 µM L-NMMA, a nitric oxide synthase (NOS) inhibitor.
Results Body weight (BW) and systolic (SBP) and diastolic (DBP) blood pressure were significantly increased in HFD dams (BW: p < 0.05, SBP: p < 0.001, DBP: p < 0.01) and their offspring at 24 weeks (BW <0.0001, SBP: p < 0.0001, DBP: p < 0.0001) compared to controls but no differences were observed in offspring at 12 weeks. PVAT exerted an anti-contractile effect in artery segments from control dams and their offspring at 12 and 24 weeks (p < 0.01, p < 0.001, p < 0.05), an effect which was lost in both dams fed HFD and their offspring. AMPK activation decreased contractility of both PVAT-denuded and intact control vessels in the presence and absence of a NOS inhibitor in control dams (p < 0.0001) and their offspring (p < 0.0001); this effect was decreased in PVAT-intact vessels of HFD dams and their offspring.
Conclusions In summary, the attenuated anti-contractile effects of PVAT in HFD dams and their offspring may be modulated by AMPK; however it is not totally dependent on nitric oxide release.
- Maternal obesity
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