Key result
ATM deficiency in mice fed a Western-type diet accelerated body weight gain and was associated with increased cardiac preload, hypertrophy, and apoptosis.
Why the study?
ATM kinase deficiency in humans associates with enhanced susceptibility to ischemic heart disease, prompting investigation into its role in diet-induced alterations in cardiac function and biochemistry.
Does ATM deficiency modulate functional and biochemical parameters of the heart in response to a Western-type diet in mice?
Does ATM deficiency modulate functional and biochemical parameters of the heart in response to a Western-type diet in mice?
ATM deficiency in mice fed a Western diet exacerbates weight gain and adverse cardiac remodeling, providing a potential mechanism for the increased susceptibility to ischemic heart disease seen in ATM-deficient patients.
Answers are grounded in this paper and cite their sources.
ATM deficiency may mediate diet-related cardiac changes in mice; hypothesis-generating and should not alter clinical practice.
Ataxia-telangiectasia mutated (ATM) kinase deficiency in humans associates with enhanced susceptibility to ischemic heart disease. Here, we provide evidence that ATM deficiency accelerates body weight gain and associates with increased cardiac preload, hypertrophy, and apoptosis in mice fed with Western-type diet (WD). Further investigations of the role of ATM deficiency in WD-induced alterations in function and biochemical parameters of the heart may provide clinically applicable information on treatment and/or nutritional counseling for patients with ATM deficiency.
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Wingard et al. (2021) studied Ataxia-telangiectasia mutated (ATM) kinase deficiency. ATM deficiency and Western-type diet was evaluated on Body weight gain, cardiac preload, hypertrophy, and apoptosis. ATM deficiency in mice fed a Western-type diet accelerated body weight gain and was associated with increased cardiac preload, hypertrophy, and apoptosis.
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