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Activation of systemic, but not local, renin-angiotensin system is associated with upregulation of TNF-a during prolonged fasting in northern elephant seal pups.
- Source :
- Journal of Experimental Biology; Sep2013, Vol. 216 Issue 17, p3215-3221, 7p
- Publication Year :
- 2013
-
Abstract
- Northern elephant seal pups naturally endure a 2-3?month post-weaning fast that is associated with activation of systemic renin-angiotensin system (RAS), a decrease in plasma adiponectin (Acrp30), and insulin resistance (IR)-like conditions. Angiotensin II (Ang II) and tumor necrosis factor-alpha (TNF-a) are potential causal factors of IR, while Acrp30 may improve insulin signaling. However, the effects of fasting-induced activation of RAS on IR-like conditions in seals are not well described. To assess the effects of prolonged food deprivation on systemic and local RAS, and their potential contribution to TNF-a as they relate to an IR condition, the mRNA expressions of adipose and muscle RAS components and immuno-relevant molecules were measured along with plasma RAS components. Mean plasma renin activity and Ang II concentrations increased by 89 and 1658%, respectively, while plasma angiotensinogen (AGT) decreased by 49% over the fast, indicative of systemic RAS activation. Prolonged fasting was associated with decreases in adipose and muscle AGT mRNA expressions of 69 and 68%, respectively, corresponding with decreases in tissue protein content, suggesting suppression of local AGT production. Muscle TNF-a mRNA and protein increased by 239 and 314%, whereas those of adipose Acrp30 decreased by 32 and 98%, respectively. Collectively, this study suggests that prolonged fasting activates a systemic RAS, which contributes to an increase in muscle TNF-a and suppression of adipose Acrp30. This targeted and tissue-specific regulation of TNF-a and Acrp30 is likely coordinated to synergistically contribute to the development of an IR-like condition, independent of local RAS activity. These data enhance our understanding of the adaptive mechanisms evolved by elephant seals to tolerate potentially detrimental conditions. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 00220949
- Volume :
- 216
- Issue :
- 17
- Database :
- Complementary Index
- Journal :
- Journal of Experimental Biology
- Publication Type :
- Academic Journal
- Accession number :
- 90278327
- Full Text :
- https://doi.org/10.1242/jeb.085225