Posted on 05/28/2023 4:10:33 PM PDT by ConservativeMind
A study conducted in mice has revealed that maternal milk provides an essential signal that triggers the maturation of heart metabolism after birth, allowing the neonatal heart to function correctly and ensuring postnatal survival.
The study shows that the fatty acid gamma-linolenic acid (GLA), present in breast milk, binds to the retinoid X receptor (RXR) protein found in heart cells. RXR acts as a nutritional sensor of lipids and vitamin A derivatives, altering gene expression and influencing biological functions such as immunity, cell differentiation, and metabolism. Once activated by maternal GLA, RXR initiates genetic programs that equip mitochondria, the energy centers of the cell, with the enzymes and other proteins they need to to start consuming lipids, the primary source of energy in the mature heart.
The results could have significant therapeutic implications for cardiovascular disorders involving mitochondrial and metabolic dysfunction, explained Dr. Mercedes Ricote.
In a mouse model, the research team found that the absence of RXR in the heart or the lack of GLA in maternal milk prevented mitochondria in the hearts of newborn mice from producing energy correctly, leading to severe heart failure and death 24 to 48 hours after birth.
The heart of a newborn mammal must quickly produce energy to sustain cardiac contraction outside of the womb. To achieve this, cardiomyocytes, the contracting cells of the myocardium (the cardiac muscle), need to activate their mitochondria to use lipids as the energy source for the generation of ATP (adenosine triphosphate—the essential energy currency of the cell). Although this process is crucial for the survival of the organism, until now, little was known about the signals that trigger the physiological adaptation of the heart after birth.
(Excerpt) Read more at medicalxpress.com ...
Either of these issues can allow this problem to occur.
At least now, this is known and GLA is easy to supplement, on its own.
Thanks!
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