It’s no secret that obesity is a growing problem in industrialized countries. In 2011 almost 35% of adults were obese and about 69% were overweight. Why obesity is a greater problem now than in the past is unclear, although it’s likely multi-factorial – less physical activity, more calorie-dense foods, chemicals in the environment that contribute to obesity, the fact that the population is aging and greater amounts of stress.
Genetics is also a factor. Some people appear to have “thrifty genes,” meaning their body is genetically predisposed to conserve energy and store fat. Having thrifty genes came in handy during periods of famine, as might have occurred during evolution, but these days when food is in abundant thrifty genes are more likely to cause problems like obesity and type 2-diabetes.
Mitochondria and Obesity: Are Obese People Different at the Cellular Level?
You might wonder whether people who are obese or prone to obesity differ physiologically from those who are lean. One area of research is looking at the role mitochondria, the energy powerhouses inside cells that produce ATP, play. ATP is the energy currency cells use to fuel muscle contraction, cellular activities and to maintain life.
Mitochondria have the task of oxidizing carbohydrates and fats to produce energy. They convert the food you eat into chemical energy your body uses to keep you running. After a meal, there are plenty of dietary sources of fat and carbohydrates mitochondria can use to make energy in the form of ATP. Also available inside muscle and liver cells are stored carbohydrates (glycogen) cells that can be converted to energy. When you don’t eat for a while and glycogen stores are depleted, fat from fat stores are sent to the mitochondria to make ATP through a process called fatty acid oxidation. You want this process to be efficient if you’re trying to shed body fat. Fortunately, healthy mitochondria are very efficient at doing this.
Do people who are obese have mitochondria that are less efficient at oxidizing fat? Some studies suggest this is the case. One study showed obese people have mitochondria that differ structurally from people of normal weight. Not only are they different in structure, but some research also shows the enzymes in mitochondria that break down fat are less active in people who are obese. One enzyme in particular called carnitine carries fatty acids from fat breakdown into the mitochondria where it can be oxidized for energy. If carnitine falls down on the job, fatty acids can’t enter the mitochondria to be oxidized. That puts a damper on your ability to burn fat. According to some studies, obese people have fewer total mitochondria inside their cells to oxidize fat.
Obesity: Obese People May Be Less Metabolically Flexible
Mitochondria also have the capacity to use glucose, from sugar and carbohydrates, to make ATP. If you eat a carbohydrate meal along with fat, your mitochondria will preferentially use glucose from the breakdown of carbohydrates before it uses fat. After a carbohydrate meal, there’s plenty of insulin around and insulin blocks the ability of mitochondria to oxidize fat. Instead, fat is funneled into storage, to places where you don’t want it like your hips, tummy, and thighs.
Once insulin drops several hours after a meal, the mitochondria can again oxidize fat as a fuel source. This is referred to as metabolic flexibility, the ability to burn carbohydrates as a fuel source when it’s available and fat when it’s not. Obese people may lack the degree of metabolic flexibility that leaner people have. Specifically, their mitochondria may be less able to oxidize fat to make ATP. As a result, fat is more likely to be stored as fat deposits.
Mitochondrial dysfunction may also partially explain why people gain body fat with age. With age, mitochondria become damaged from oxidative stress and the natural aging process. As mitochondria accumulate greater amounts of damage, they have a harder time oxidizing fat and converting it into energy.
Obesity: Can You Improve the Health of Your Mitochondria?
If you want to be an efficient fat burner, you need healthy mitochondria and enough of them to oxidize fat efficiently. One way to increase the number of mitochondria inside your muscle cells is through aerobic exercise. As you know, exercise is a stress that causes your body to adapt. One way it adapts to aerobic activity is to increase the number of energy-producing mitochondria inside cells and by ramping up production of mitochondria enzymes that oxidize fat. It does this to give cells the ability to produce more ATP to fuel exercise.
Another way to “force” mitochondria to oxidize fat is to deprive cells of carbohydrate, the fuel they preferentially use to make ATP. This could be accomplished by eating a relatively low-carbohydrate diet so cells have to oxidize fat for fuel instead of carbohydrates. Some research shows low-carb diets are effective for weight loss in people who are obese.
Oxidative stress may damage mitochondria and reduce their ability to function. This raises the question as to whether dietary antioxidants might reduce oxidative damage and preserve mitochondrial function. Just as our bodies age, so do the mitochondria inside cells that keep them running. Some experts propose that the antioxidant coenzyme Q10 may help. In animals, coenzyme Q10 protects cells against damage due to toxins that target the mitochondria. In addition, regular aerobic exercise up-regulates the body’s antioxidant defense system for greater protection against oxidative damage.
The Bottom Line?
Mitochondria play a role in overall health and when they don’t function properly, they may play a role in aging and obesity. There’s no magical way to repair poorly functioning mitochondria, although aerobic exercise and a diet rich in antioxidants may help. It will be interesting to see what future research shows about the role, if any, mitochondria play in regulating body weight.
References:
Low Carb for You. “Impaired Mitochondrial Function and Obesity, Part 2” November 11, 2011.
The State of Obesity. “Obesity Rates & Trends Overview”
Curr Opin Endocrinol Diabetes Obes. 2010 Oct;17(5):446-52. doi: 10.1097/MED.0b013e32833c3026.
Diabetes January 2005 vol. 54 no. 1 8-14.
Mayo Clinic. “Coenzyme Q10”
European Journal of Applied Physiology
April 2009, Volume 105, Issue 6, pp 861-867.
Am J Clin Nutr January 2009 vol. 89 no. 1 467S-471S.
Possible Health Benefits of Coenzyme Q10. Roland Stocker, Ph.D. University of New South Wales. Sydney, Australia.
Diabetes and Vascular Disease Research May 2006 vol. 3 no. 1 7-11.
Ann N Y Acad Sci. 2002 Apr;959:82-92.
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The Role Mitochondria Play in Healthy Aging and How Exercise Keeps Them Healthy
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