Angiotensin II and the development of insulin resistance: Implications for diabetes

Olivares-Reyes, J. Alberto; Arellano-Plancarte, Araceli; Castillo-Hernández, Jesús

doi:10.1016/j.mce.2008.12.011

Cited by 165 publications

(183 citation statements)

References 131 publications

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“…While increased Ang II can activate adipose cytokines such as TNF-α and IL-6 (Olivares- Reyes et al, 2009;Skurk et al, 2004), it can simultaneously decrease plasma Acrp30 concentrations in rats (Ran et al, 2006). In the present study, prolonged fasting decreased adipose Acrp30 mRNA expression, which coincides with the previously demonstrated decrease in plasma Acrp30 after 8weeks of fasting in elephant seals (Viscarra et al, 2011a).…”

Section: Discussionsupporting

confidence: 90%

“…Inappropriate activation of systemic and local RAS, when associated with obesity, contributes to insulin resistance through cytokine expression (Dandona et al, 2007;Henriksen, 2007;Kalupahana and Moustaid-Moussa, 2012;Karlsson et al, 1998;Olivares-Reyes et al, 2009;Shiuchi et al, 2004). Angiotensin (Ang) II activates tissue-derived cytokines such as TNF-α in adipose and muscle tissue (Kurata et al, 2006;Wei et al, 2008b).…”

Section: Introductionmentioning

confidence: 99%

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Activation of systemic, but not local, renin-angiotensin system is associated with up-regulation of TNF-α during prolonged fasting in northern elephant seal pups

Suzuki

Vázquez‐Medina

Viscarra

et al. 2013

Journal of Experimental Biology

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SUMMARYNorthern 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-α) 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-α 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-α 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-α and suppression of adipose Acrp30. This targeted and tissue-specific regulation of TNF-α 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.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Activation of systemic, but not local, renin-angiotensin system is associated with up-regulation of TNF-α during prolonged fasting in northern elephant seal pups

Suzuki

Vázquez‐Medina

Viscarra

et al. 2013

Journal of Experimental Biology

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“…7,8 Angiotensin II plays an important role in the pathogenesis of insulin resistance at least in part because of enhanced inflammation and oxidative stress via angiotensin II type 1 (AT 1 ) receptor stimulation. 9,10 We demonstrated previously that an AT 1 receptor blocker (ARB) ameliorated insulin resistance in a T2DM mouse model, KK-Ay 11 ; however, the association between low-grade inflammation and the efficacy of ARB to attenuate insulin resistance is still unclear.…”

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confidence: 99%

Roles of Interleukin 17 in Angiotensin II Type 1 Receptor–Mediated Insulin Resistance

et al. 2012

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Abstract-Interleukin 17 (IL-17) is known to contribute to the pathogenesis of hypertension, atherosclerosis, and adipocyte differentiation; however, the roles of IL-17 in glucose metabolism remain to be elucidated. Angiotensin II type 1 receptor blockers improve insulin resistance at least in part because of the amelioration of inflammation. Therefore, we examined the possible roles of IL-17 in the pathogenesis of insulin resistance in type 2 diabetes mellitus using a mouse model, KK-Ay, and angiotensin II type 1 receptor-mediated insulin resistance. KK-Ay mice were administered control-IgG 2A or anti-IL-17 antibody 5 times at a dose of 100 g every second day by IP injection. KK-Ay mice were administered telmisartan for 2 weeks. C57BL/6J mice treated with angiotensin II infusion for 2 weeks were administered telmisartan or hydralazine. Insulin resistance was evaluated by oral glucose tolerance test, insulin tolerance test, and uptake of 2-

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“…27 A final proposed mechanism is that low sodium intake alters the level of angiotensin II, which regulates insulin activity. 28 These proposed mechanisms all suggest that lower dietary sodium intake is associated with human glucose and insulin metabolism and could further help to prevent diabetes mellitus and metabolic syndrome. In the present study, we did not assess insulin resistance because we had limited information on blood glucose level.…”

Section: Discussionmentioning

confidence: 99%

The association between dietary sodium intake and adiposity, inflammation, and hormone markers: A preliminary study

Choi

Heo

2017

J Nutr Health

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Purpose: Excess intake of sodium is a major diet-related risk factor for human diseases including hypertension and cancer as well as obesity and inflammation. However, findings are still controversial, and evidence is lacking in Koreans. Therefore, for better understanding of the role of dietary sodium intake in disease etiology, this study investigated the effects of dietary sodium intake on adiposity, inflammation, and hormones in Koreans. Methods: A total of 80 males and females joined the study. The general characteristics and dietary intake data were investigated by trained interviewers using a questionnaire and 24-h dietary recall, respectively. For the markers of adiposity, body weight, body mass index, percent of body fat, visceral fat area, and waist and hip circumference were measured. For the inflammation and hormone markers, leptin, adiponectin, insulin, tumor necrosis factor-α, and interleukin-6 were also analyzed. Results: Multivariate linear regression analyses suggested that dietary sodium intake was not associated with adiposity. However, dietary sodium showed a significant association with insulin level: Plasma insulin concentration increased with sodium intake independent of other dietary intake or percent of body fat (β = 0.296, adjusted r 2 = 0.276, p < 0.01). Other markers for inflammation and hormonal responses were not associated with dietary sodium intake. Conclusion: Findings suggested that dietary sodium intake may be a critical modifying factor in the level of plasma insulin. However, it showed a limited effect on obesity and other inflammation markers and hormone levels. These findings should be confirmed in larger, well-designed investigations.

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Angiotensin II and the development of insulin resistance: Implications for diabetes

Cited by 165 publications

References 131 publications

Activation of systemic, but not local, renin-angiotensin system is associated with up-regulation of TNF-α during prolonged fasting in northern elephant seal pups

Activation of systemic, but not local, renin-angiotensin system is associated with up-regulation of TNF-α during prolonged fasting in northern elephant seal pups

Roles of Interleukin 17 in Angiotensin II Type 1 Receptor–Mediated Insulin Resistance

The association between dietary sodium intake and adiposity, inflammation, and hormone markers: A preliminary study

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