Age-related metabolic diseases may prevent with fatty acid-binding proteins

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age-related metabolic diseases

Age-related metabolic diseases

A range of age-related metabolic diseases may prevent by lowering the levels of certain proteins called fatty acid-binding proteins (FABPs).

A new study suggests, metabolic health may preserve well into old age, if we keep fatty acid-binding protein levels very low. These proteins tasked with “grabbing” fat molecules and “guiding” them within the cell.

FABPs involved in the metabolism, signaling, and trafficking of lipids, and they found in abundance in the heart and liver tissue, where there is a highly active fatty acid metabolism.

In the new study, researchers from the Harvard T.H. Chan School of Public Health, found that mice that lack FABPs exhibit substantial protection against obesity, inflammation, insulin resistance, type-2 diabetes, and fatty liver disease as they age compared with mice that have FABPs. This remarkable extension of metabolic health not found to lengthen lifespan.

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High-calorie diet slows down metabolism

Researchers suggested that a high-calorie diet slows down metabolism and accelerates the aging process. Calorie restriction has shown to slow down aging and protect against age-related metabolic diseases.

This observation reveals in early 1935. Researchers still trying to study the mysterious mechanism behind the benefits of calorie restriction. Also, it is unclear if the preservation of cardio metabolic health sufficient extends lifespan.

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To find out, researchers genetically engineered mice lacked FABPs. These mice shared molecular and lipidomic features with mouse models of calorie restriction.

In previous work, researchers found that mice with deficient levels of FABPs fed a high diet in fat or cholesterol did not develop cardio-metabolic diseases.

The researchers designed several cohorts of FABP-deficient rodents and followed them throughout their lives.

The study found that insufficient FABP levels extended metabolic health span, protecting against insulin resistance and glucose intolerance, inflammation, deterioration of adipose tissue integrity, and fatty liver disease.

These data indicate that extension of the metabolic health span in the absence of calorie restriction can uncouple from lifespan, indicating the potential for independent drivers of these pathways.

These simple proteins carry many fascinating mysteries that could unlock some of the greatest challenges to human health.

More information: [Cell Reports]

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