What is the clinical evidence from this study?

Study design: Other. Population: Polycystic ovary syndrome (PCOS) (n=32). Intervention: Angiotensin 1-7 (Ang 1-7) vs. Vehicle. Primary outcome: Cardiometabolic complications (food intake, body and fat depot weight, glucose tolerance, adipokines, MAP).

What does this research mean for the field?

Angiotensin 1-7 fails to counteract hyperandrogenemia-mediated cardiometabolic complications, such as obesity and hypertension, in a rat model of polycystic ovary syndrome, despite mitigating early-phase glucose intolerance. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

June 7, 2026

2443-P: Effect of Angiotensin 1-7 on the Cardiometabolic Complications in a Rat Model of PCOS

Key Result

In a rat model of PCOS, Ang-(1-7) mitigated early-phase glucose intolerance but failed to treat DHT-induced obesity, hypertension, or adiponectin suppression.

Key Points

This study aims to evaluate if angiotensin 1-7 can mitigate hyperandrogenemia-induced cardiometabolic issues in a polycystic ovary syndrome model.
Four-week-old female Sprague-Dawley rats (n=8/group) received DHT implants with vehicle or angiotensin 1-7 (500 µg/kg/day) via sc minipump.
Food intake, body and fat depot weight, glucose tolerance, circulating adipokines, and mean arterial pressure were measured.
Data were analyzed using two-way ANOVA (p<0.05).
DHT increased food intake, body weight, and fat depots weights (1.2-3.6-fold) and decreased adiponectin levels by 66%.
Ang 1-7 reduced leptin and adiponectin levels significantly by 89% and 55%, respectively; DHT blunted these effects.
DHT increased MAP to 109 ± 2 mmHg, but Ang 1-7 did not affect MAP.

Structured PICO

Does Angiotensin 1-7 mitigate hyperandrogenemia-induced cardiometabolic complications in a rat model of PCOS?

Population

32 four-week-old female Sprague-Dawley rats in a DHT-induced PCOS model treated with Ang 1-7 or vehicle.

Intervention

Angiotensin 1-7 (500 µg/kg/day, sc minipump)

Comparator

Vehicle

Outcome

Cardiometabolic complications including food intake, body and fat depot weight, glucose tolerance, circulating adipokines, adipose adipokines mRNA, and mean arterial pressuresurrogate

In a rat model of PCOS, Angiotensin 1-7 improved early-phase glucose intolerance but did not reverse hyperandrogenemia-induced obesity, hypertension, or adiponectin suppression.

Abstract

Introduction and Objective: Polycystic ovary syndrome (PCOS) is characterized by hyperandrogenism and high prevalence of cardiometabolic complications in women. The renin-angiotensin system (RAS) regulates cardiometabolic homeostasis through opposing actions of angiotensin II (Ang II) and angiotensin 1-7 (Ang 1-7), which promote injury and protection, respectively. In PCOS, androgen-driven Ang II activation contributes to cardiometabolic dysfunction. Whether Ang 1-7 counteracts these effects remains unclear. We aim to determine if administration of Ang 1-7 mitigates hyperandrogenemia-induced cardiometabolic complications in a PCOS model. Methods: Four-week-old female Sprague-Dawley rats (n=8/group) received empty or dihydrotestosterone (DHT) implants (8 mg, sc) with vehicle or Ang 1-7 (500 µg/kg/day, sc minipump). Food intake, body and fat depot weight, glucose tolerance (oral glucose tolerance test), circulating adipokines (ELISA), and adipose adipokines mRNA (RT-qPCR) were measured. Mean arterial pressure (MAP) was measured by radiotelemetry. Data were analyzed using two-way ANOVA (p0.05). Results: DHT significantly increased food intake, body weight, and fat depots weights (1.2-3.6-fold), and significantly decreased adiponectin levels by 66%. Ang-1-7 reduced leptin and adiponectin levels by 89% and 55%, respectively, and decreased their adipose mRNA expression by 85-90% and 55-70%, respectively; an effect that was blunted by DHT. DHT increased early-phase glucose levels in OGTT (15 min), an effect prevented by Ang 1-7, however, the overall area under the curve was not changed. DHT significantly increased MAP compared to control in vehicle-treated groups (109 ± 2 vs. 103 ± 1 mmHg), but Ang 1-7 did not affect MAP. Conclusion: Ang-(1-7) successfully mitigated early-phase glucose intolerance, but failed to treat the DHT-induced obesity, hypertension, or the suppression of adiponectin in a model of PCOS. Ang-(1-7) failed to counteract the hyperandrogenemia-mediated Ang II-induced cardiometabolic complications in PCOS. Disclosure M.A. Eissa: None. K.M. Thompson: None. S. Rezq: None. N. Shawky Elsayed: None. D.G. Romero: None. L.L. Yanes Cardozo: None. Funding American Diabetes Association (1-26-PDF-0678)

Ask AI

Helpful

Bookmark