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Amyloid beta 42 alters cardiac metabolism and impairs cardiac function in male mice with obesity
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Amyloid beta 42 alters cardiac metabolism and impairs cardiac function in male mice with obesity
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Journal Article
Amyloid beta 42 alters cardiac metabolism and impairs cardiac function in male mice with obesity
2024
Overview
There are epidemiological associations between obesity and type 2 diabetes, cardiovascular disease and Alzheimer’s disease. The role of amyloid beta 42 (Aβ
42
) in these diverse chronic diseases is obscure. Here we show that adipose tissue releases Aβ
42
, which is increased from adipose tissue of male mice with obesity and is associated with higher plasma Aβ
42
. Increasing circulating Aβ
42
levels in male mice without obesity has no effect on systemic glucose homeostasis but has obesity-like effects on the heart, including reduced cardiac glucose clearance and impaired cardiac function. The closely related Aβ
40
isoform does not have these same effects on the heart. Administration of an Aβ-neutralising antibody prevents obesity-induced cardiac dysfunction and hypertrophy. Furthermore, Aβ-neutralising antibody administration in established obesity prevents further deterioration of cardiac function. Multi-contrast transcriptomic analyses reveal that Aβ
42
impacts pathways of mitochondrial metabolism and exposure of cardiomyocytes to Aβ
42
inhibits mitochondrial complex I. These data reveal a role for systemic Aβ
42
in the development of cardiac disease in obesity and suggest that therapeutics designed for Alzheimer’s disease could be effective in combating obesity-induced heart failure.
Epidemiological evidence has identified associations among obesity, Alzheimer’s disease, and cardiovascular disease. Here, the authors report that adipose tissue releases amyloid beta 42 (Aβ42) and that antagonizing Aβ42 protects cardiac function in obesity murine models.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
