4 results match your criteria: "Department of Pharmacology and Nutritional Sciences University of Kentucky Lexington KY.[Affiliation]"

Article Synopsis
  • - The study explored how early life stress from maternal separation and early weaning (MSEW) impacts blood pressure in obese male mice, focusing on the role of the renin-angiotensin-aldosterone system.
  • - Both control and MSEW mice on a high-fat diet showed similar increases in angiotensinogen levels, but there was no activation of the renin-angiotensin system in their fat or kidneys.
  • - Despite a reduction in blood pressure after treating with an angiotensin-converting enzyme inhibitor, MSEW mice still experienced heightened sympathetic tone, indicating that other mechanisms beyond angiotensin II contribute to their elevated blood pressure.
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Background Mitochondrial dysfunction contributes to the cardiac remodeling triggered by type 2 diabetes (T2D). Mitochondrial Ca concentration ([Ca]) modulates the oxidative state and cytosolic Ca regulation. Thus, we investigated how T2D affects mitochondrial Ca fluxes, the downstream consequences on myocyte function, and the effects of normalizing mitochondrial Ca transport.

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Background We have previously reported that female mice exposed to maternal separation and early weaning (MSEW), a model of early life stress, show exacerbated diet-induced obesity associated with hypertension. The goal of this study was to test whether MSEW promotes angiotensin II-dependent hypertension via activation of the renin-angiotensin system in adipose tissue. Methods and Results MSEW was achieved by daily separations from the dam and weaning at postnatal day 17, while normally reared controls were weaned at postnatal day 21.

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Background Obesity-associated chronic inflammation has been known to contribute to atherosclerosis development, but the underlying mechanisms remain elusive. Recent studies have revealed novel functions of IKK β (inhibitor of NF -κB [nuclear factor κB] kinase β), a key coordinator of inflammation through activation of NF -κB, in atherosclerosis and adipose tissue development. However, it is not clear whether IKK β signaling in adipocytes can also affect atherogenesis.

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