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Enzyme could help fight against mid-life obesity

A team from the National Institutes of Health has identified an enzyme working against us in the battle over mid-life obesity and loss of fitness. The discovery in mice could change current ideas of why we gain weight as we age. It might also influence pregnancy attempts for mid-life women.


"Our society attributes the weight gain and lack of exercise at mid-life (approximately 30-60 years) primarily to poor lifestyle choices and lack of will power, but this study shows there is a genetic program driven by an overactive enzyme that promotes weight gain and loss of exercise capacity at mid-life," says lead author Jay H. Chung, PhD, MD, head of the Laboratory of Obesity and Aging Research at the National Heart, Lung, and Blood Institute (NHLBI), part of  the National Institutes of Health in America.


Mice tested the potentially key role DNA-PK plays in obesity and exercise capacity. An inhibitor blocking the enzyme was given to one group being fed high-fat foods, and withheld in another. The group receiving the DNA-PK inhibitor had a 40 % decrease in weight gain.


The study, the first to link increased activity of this enzyme to aging and obesity, appears in the current issue of Cell Metabolism. Its findings could have significant affect on several chronic illnesses including heart disease, diabetes, cancers, Alzheimer's disease, and other diseases tending to increase with age or impede other metabolic recovery systems.

Researchers have known for years that losing weight and maintaining the capacity to exercise gets harder beginning between ages 30 to 40 — the start of mid-life. Although science has developed new therapies for obesity, including fat-fighting pills, many therapies fail with the lack of understanding about biological changes causing middle-aged weight gain, particularly weight around the abdomen.

Chung as an endocrinologist, was always puzzled by the aging-weight gain paradox. An average adult in America gains 30 pounds from age 20 to 50, even though food intake usually decreases during this time. His aim in the current study was to better understand why mid-life weight gain occurs and lowers exercise capacity. He and his associates searched for biochemical changes occurring in middle-aged animals (human equivalent of 45 years) and found an enzyme called DNA-dependent protein kinase, or DNA-PK, increases its activity with age.


DNA-PK promotes conversion of nutrients to fat storage, while decreasing mitochondria — the tiny organelles in cells that turn fat into energy.

Mitochondria are found abundant among young people, but drop considerably in older people. Research shows decreased mitochondria can promote obesity and a loss of exercise capacity.


Chung and his associates theorized that reducing DNA-PK activity may decrease fat accumulation and increase mitochondria number as well as promote fat burning. The researchers tested their theory in mice by orally administering a drug that inhibits DNA-PK. They found in addition to preventing weight gain in the mice, the inhibitor boosted mitochondrial content in skeletal muscle, increased aerobic fitness in obese and middle aged mice, and reduced the incidence of obesity and type-2 diabetes.


"Our studies indicate DNA-PK is one of the drivers of metabolic and fitness decline that occurs during aging, which makes staying lean and physically fit difficult and increases susceptibility to metabolic diseases like diabetes.

"The identification of this new mechanism is very important for improving public health. The study opens the door to the development of a new type of weight-loss medication that could work by inhibiting DNA-PK activity."


Jay H. Chung, PhD, MD, Head of Laboratory of Obesity and Aging Research, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA


However, he notes that DNA-PK inhibitors have yet to be tested this way in humans. In the meantime, researchers encourage middle-aged people to fight obesity with common practices of reducing calorie intake and boosting exercise, even if it takes a while to see results.

Highlights
•Aging increases DNA DSBs and DNA-PK phosphorylation of HSP90α in skeletal muscle
•HSP90α phosphorylation disrupts HSP90α chaperone function for the AMPK pathway
•Inhibiting HSP90α phosphorylation prevents loss of AMPK activity and mitochondria
•Inhibiting DNA-PK ameliorates obesity, type 2 diabetes and physical decline

Summary
Hallmarks of aging that negatively impact health include weight gain and reduced physical fitness, which can increase insulin resistance and risk for many diseases, including type 2 diabetes. The underlying mechanism(s) for these phenomena is poorly understood. Here we report that aging increases DNA breaks and activates DNA-dependent protein kinase (DNA-PK) in skeletal muscle, which suppresses mitochondrial function, energy metabolism, and physical fitness. DNA-PK phosphorylates threonines 5 and 7 of HSP90α, decreasing its chaperone function for clients such as AMP-activated protein kinase (AMPK), which is critical for mitochondrial biogenesis and energy metabolism. Decreasing DNA-PK activity increases AMPK activity and prevents weight gain, decline of mitochondrial function, and decline of physical fitness in middle-aged mice and protects against type 2 diabetes. In conclusion, DNA-PK is one of the drivers of the metabolic and fitness decline during aging, and therefore DNA-PK inhibitors may have therapeutic potential in obesity and low exercise capacity.

This study was supported by the Intramural Research Program of NHLBI, part of NIH.

About NHLBI: Part of the National Institutes of Health, the National Heart, Lung, and Blood Institute (NHLBI) plans,conducts, and supports research related to the causes, prevention, diagnosis,and treatment of heart, blood vessel, lung, and blood diseases; and sleep disorders. The Institute also administers national health education campaigns on women and heart disease, healthy weight for children, and other topics. NHLBI press releases and other materials are available online at http://www.nhlbi.nih.gov.

About the National Institutes of Health (NIH): NIH, the nation's medical research agency,includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.
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3-D image of the enzyme DNA-PK. Study in animals shows
inhibiting this enzyme may help fight obesity.
Image Credit:
NHLBI

 


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