Key result
A high-fat diet and streptozotocin-induced metabolic syndrome model (systolic BP 154 vs 110 mmHg) resulted in greater vascular dysfunction and structural abnormalities in the abdominal aorta.
Why the study?
It was unknown whether aortic dysfunction in metabolic syndrome is expressed uniformly across both the thoracic and abdominal aorta.
Does metabolic syndrome differentially affect the functional and structural properties of the thoracic and abdominal aorta in a rat model?
Does metabolic syndrome differentially affect the functional and structural properties of the thoracic and abdominal aorta in a rat model?
In a rat model of metabolic syndrome, functional and structural vascular abnormalities are more severe in the abdominal aorta than the thoracic aorta.
Hypothesis-generating for metabolic contributions to aortic pathology; leaves open translation to human hypertension and diabetes.
NEW FINDINGS: What is the central question of this study? Is aortic dysfunction, a significant contributor to cardiovascular disease in metabolic syndrome, expressed uniformly across both the thoracic and abdominal aorta? What is the main finding and its importance? Our study shows that, in the setting of metabolic syndrome, functional and structural deficits in the aorta are differentially expressed along its length, with the abdominal portion displaying more extensive vascular abnormalities. It is, therefore, likely that early interventional strategies targeting the abdominal aorta might alleviate cardiovascular pathologies driven by the metabolic syndrome. ABSTRACT: The extent of vascular dysfunction associated with metabolic syndrome might vary along the length of the aorta. In this study, we investigated regional functional and structural changes in the thoracic and abdominal aorta of a rat model of metabolic syndrome, namely, high-fat diet (HFD) streptozotocin-induced diabetes mellitus (HFD-D). Four-week-old male Wistar albino rats were fed with either HFD or control diet (CD) for 10 weeks. At week 6, 40 mg/kg streptozotocin and its vehicle were injected i.p. into HFD and CD groups, respectively. At the end of the feeding period, rats were euthanised and aortic segments collected for assessment of vascular functional responses and histomorphometry. Tail-cuff systolic blood pressures (154 ± 6 vs. 110 ± 4 mmHg) and areas under the curve for oral glucose and i.p. insulin tolerance tests were greater in HFD-D versus CD rats. Abdominal aortic vasoconstriction in response to noradrenaline and KCl was greater in HFD-D compared with CD rats. Thoracic vasoconstrictor responses to noradrenaline, but not KCl, were greater in the HFD-D group. Abdominal, but not thoracic, endothelium-dependent vasorelaxation in response to acetylcholine was blunted in HFD-D relative to CD rats; however, nitric oxide-dependent vasorelaxation in HFD-D rats was impaired in both thoracic and abdominal segments. The abdominal aorta of HFD-D rats showed deranged interlamellar spacing and increased lipid plaque deposition. In conclusion, vascular dysfunction in metabolic syndrome is expressed differentially along the length of the aorta, with the abdominal aorta exhibiting increased susceptibility to vasoconstrictors and greater deficits in endothelium-dependent relaxation. These vascular functional abnormalities could potentially underlie the development of hypertensive cardiovascular disease associated with the metabolic syndrome.
No takes yet. Share an insight, caveat, or question.
Ameer et al. (2021) studied Metabolic syndrome. High-fat diet and streptozotocin vs. Control diet and vehicle was evaluated on Regional functional and structural changes in the thoracic and abdominal aorta. A high-fat diet and streptozotocin-induced metabolic syndrome model (systolic BP 154 vs 110 mmHg) resulted in greater vascular dysfunction and structural abnormalities in the abdominal aorta.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: