Why the study?
Although cardiac mitochondrial Akt1 activation modulates metabolic homeostasis, the underlying mechanism is incompletely understood, prompting investigation into whether gut microbiota mediates these benefits.
Does gut microbiota depletion with broad-spectrum antibiotics negate the metabolic benefits of cardiac mitochondrial Akt1 activation in a mouse model of diet-induced diabetic cardiomyopathy?
Population
Inducible myocardium-specific transgenic mice (CAMCAKT) fed a high fat-high fructose diet
Comparison
Antibiotic-treated CAMCAKT mice vs untreated CAMCAKT mice and non-induced controls
Design
Transgenic animal study
Follow-up
2 months
Key result
Microbiota depletion with antibiotics negated the metabolic benefits of cardiac mitochondrial Akt1 activation, resulting in 7% higher body fat mass compared to controls.
Authors
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No practice change warranted from this animal model; leaves open microbiota mediation of cardiac Akt1 metabolic effects in diabetic cardiomyopathy.
Does gut microbiota depletion with broad-spectrum antibiotics negate the metabolic benefits of cardiac mitochondrial Akt1 activation in a mouse model of diet-induced diabetic cardiomyopathy?
Gut microbiota depletion negates the metabolic and hepatoprotective benefits of cardiac mitochondrial Akt1 activation in a mouse model of diet-induced diabetic cardiomyopathy.
Pathak et al. (2026) studied Diet-Induced Diabetic Cardiomyopathy. Broad-spectrum antibiotics (Ampicillin and Enrofloxacin) vs. Untreated CAMCAKT mice and non-induced vehicle injected controls was evaluated on Body fat mass. Microbiota depletion with antibiotics negated the metabolic benefits of cardiac mitochondrial Akt1 activation, resulting in 7% higher body fat mass compared to controls.
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