Thursday 28 July 2016

Obesity Management In Osteoarthritis

“We know that obesity is the number-one preventable risk factor for osteoarthritis but it hasn’t been studied much because everyone dismissed it as overloading joints,”

He and others began to wonder whether obesity alone told the whole story of joint destruction. Some athletic endeavors put greater biomechanical forces on knees than obesity. And, people who are obese are more likely to have osteoarthritis (OA) in their wrists, fingers and hands. Our hands sometimes bear loads (think of carrying a heavy flower pot) but not our body weight (we don’t walk on our hands).

  overweight as to be deemed obese (defined as twenty pounds heavier than your upper weight range), those excess pounds of fat carry hidden dangers.

Fat, or adipose tissue in medical lingo, is home to millions upon millions of busy adipocytes, or fat cells. A flurry of research over the past few years is starting to explain how adipocytes work against the body to destroy joints by misguided responses to high levels of glucose and exposure to cytokines (immune proteins). In reaction to such exposure, adipocytes churn out high levels of their own immune proteins called adipokines.

Year after year of obesity fuels a steady barrage of friendly fire that in turn generates low-level chronic inflammation. Not an inflamed immune system, like an infection but a soft drum-beat of immune proteins that over time can damage tissues such as joints,

To study the link between a disrupted metabolic system and osteoarthritis,   In work recently published in Arthritis Research and Therapy, Mooney’s team studied whether a high-fat diet in diabetic mice would damage joints.

One group of mice ate a high-fat diet and then had surgery that mimics knee injuries in people and is designed to quickly bring on osteoarthritis. The second group of mice ate regular mouse chow until they had the surgery, and then ate the high-fat diet after surgery. At monthly intervals, the team examined bone and cartilage tissues in the knee joints for markers that would reveal signs of osteoarthritis.

The mice fed the high-fat diet before and after surgery ended up with a body weight considered obese; mice fed the high-fat diet after surgery gained more weight than controls but were not obese.
  with abnormal changes to their metabolism and early signs of OA. As it turns out, obesity alone wasn’t enough to damage joints; even mice that weighed less had changes in their joint tissue that showed the progression to OA. In all mice, such metabolic disturbances occurred long before mice gained a lot of weight.

 “These results argue that all you need is metabolic changes. You don’t need gross weight gain to have changes in the progression of osteoarthritis,” says Mooney. 

Next Mooney’s team will try and decipher the molecular pathways that lead from metabolic disturbances to joint damage. Mooney will also use his expertise in diabetes to see whether insulin resistance – a condition in which the tissues don’t respond to insulin well and thus can’t lower blood sugar – plays a role in damaging joints. These efforts may bring to light a potential therapy; perhaps correcting diabetes and correct insulin resistance will slow down progression to OA,  
The link between obesity and OA is actually very complicated. Adipocytes secrete many adipokines, one of which includes leptin, which regulates metabolism and body weight. Researchers need to figure out whether leptin and its protein cousins can damage cartilage directly or whether they recruit other cells for their dirty work.   they discovered that many are exactly the same immune proteins that OA researchers have been studying for years, “and no one had put them together to say all of the stuff in your joints may be coming from the fat,

As it happens, mice love to run, so the team gave some of the mice on the high-fat diet access to a running wheel; the other mice on the high fat diet didn’t run at all. All of the mice ended up obese, even mice that ran the equivalent of two miles each night. But tests on the mice that were allowed exercise showed that exercise alone slowed down the immune proteins that lead to inflammation, and reduced the severity of OA.

AFTER TRANSFORMATION



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