What question did this study set out to answer?

To determine whether chronic administration of angiotensin-(1-7) attenuates cardiac remodeling and suppresses growth-promoting intracellular signaling pathways in a fructose-fed rat model of insulin resistance.

January 8, 2010AJP Heart and Circulatory Physiology

Angiotensin-(1–7) improves cardiac remodeling and inhibits growth-promoting pathways in the heart of fructose-fed rats

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Why the study?

Does Angiotensin-(1-7) improve cardiac remodeling and inhibit growth-promoting pathways in fructose-fed rats?

Population

Sprague-Dawley rats fed either normal rat chow or the same diet plus 10% fructose in drinking water for 6…

Comparison

Angiotensin- (100 ng.kg.min) delivered via… vs Sham surgery in subgroups of control and…

Design

Preclinical

Follow-up

2 weeks of treatment

Authors

JGJorge F. GianiCedars-Sinai Medical Center MMMarina C. MuñozInstituto de Química y Fisicoquímica Biológicas MMMarcos MayerUniversity of Buenos Aires

Discussion

Member takes

Implication

Hypothesis-generating in fructose-fed rats; clinical translation of ANG-(1-7) for metabolic remodeling remains untested.

Key Points

To determine whether chronic administration of angiotensin-(1-7) attenuates cardiac remodeling and suppresses growth-promoting intracellular signaling pathways in a fructose-fed rat model of insulin resistance.
Sprague-Dawley rats received either a standard diet or a diet supplemented with 10% fructose in drinking water for 6 weeks.
During the final 2 weeks of dietary intervention, rats received continuous subcutaneous infusions of angiotensin-(1-7) (100 ng·kg⁻¹·min⁻¹) via osmotic mini-pumps or underwent sham surgery.
Assessed blood pressure, heart-to-body weight ratio, myocyte diameter, cardiac interstitial fibrosis, and phosphorylation levels of ERK1/2, JNK1/2, and p38MAPK.
Chronic angiotensin-(1-7) infusion significantly lowered fructose-induced mild hypertension and improved elevated heart-to-body weight ratio, myocyte diameter, and left ventricular fibrosis, despite circulating and local angiotensin II remaining elevated.
Angiotensin-(1-7) significantly attenuated the hyperphosphorylation of ERK1/2, JNK1/2, and p38MAPK in fructose-fed hearts, an effect associated with normalized SHP-1 protein-tyrosine phosphatase activity.

Structured PICO

Does Angiotensin-(1-7) improve cardiac remodeling and inhibit growth-promoting pathways in fructose-fed rats?

Population

Sprague-Dawley rats fed either normal rat chow (control) or the same diet plus 10% fructose in drinking water (fructose-fed rats, FFR) for 6 weeks

Intervention

Angiotensin-(1-7) (100 ng.kg(-1).min(-1)) delivered via osmotic pumps for the last 2 weeks of the 6-week diet period

Comparator

Sham surgery in subgroups of control and fructose-fed rats

Outcome

Cardiac remodeling (heart weight, myocyte diameter, interstitial fibrosis, perivascular collagen type III deposition) and growth-promoting signaling pathways (phosphorylation degree of ERK1/2, JNK1/2, and p38MAPK)surrogate

Chronic ANG-(1-7) treatment ameliorates cardiac hypertrophy, fibrosis, and growth-promoting pathways in an insulin-resistant rat model.

Cite This Study

Giani et al. (2010) studied this question.

synapsesocial.com/papers/6a702b3f2163a0a01bc462ff https://doi.org/10.1152/ajpheart.00803.2009

Topics

Hypertension management

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Angiotensin-(1–7) improves cardiac remodeling and inhibits growth-promoting pathways in the heart of fructose-fed rats

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Topics

Angiotensin-(1–7) improves cardiac remodeling and inhibits growth-promoting pathways in the heart of fructose-fed rats

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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Topics

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