The relation between obesity and osteoarthritis may be more than simply the wear and tear on the skeleton caused by extra weight. Experts from the Duke University claim to have discovered that the absence of the appetite hormone leptin could verify whether obese mice suffer from arthritis, no matter how bulky they are.
It was completely surprising to find that mice that became extremely obese had no arthritis if their bodies didn’t have leptin. This was mentioned by Farshid Guilak, PhD, director of orthopaedic study in the Duke Department of Surgery.
In fact the joints from the obese mice in the study apparently seemed better as compared to the usual control mice.
Guilak commented, “However, in another study, we found that mice that gained half as much weight on a high-fat diet but processed leptin normally showed significant knee osteoarthritis.”
Leptin may influence several factors caught up in osteoarthritis i.e. body weight, inflammation, sex hormone levels, and bone metabolism. This was the opinion of lead author Tim Griffin, PhD, who was at Duke Orthopaedic Department and now is an assistant member of the Free Radical Biology and Aging Program at the Oklahoma Medical Research Foundation.
Tim Griffin, mentioned, “That also makes leptin challenging to study, however, because it’s difficult to isolate which pathway is being altered to prevent the development of osteoarthritis.”
Leptin is said to be a familiar monitor of appetite, but this is claimed to be the first time where experts have accounted a function for leptin as a metabolic connection between obesity and changed cartilage metabolism in joints. The function of obesity as a threat issue for arthritis may be well described, but it was supposedly considered to be only a case of overloading joints with additional weight.
Guilak remarked, “It hadn’t been studied beyond that. We knew from other studies that obese people got arthritis in their hands, too, which don’t bear weight. This indicated that something besides just body-weight level affected their joints.”
The Duke team apparently embarks to study whether the augmented body fat of obesity may be the reason for inflammatory response in joints i.e. an imbalance of the immune system signaling proteins known as cytokines and other chemicals in osteoarthritis.
It was learnt by the experts that mice were apparently leptin-deficient or deficient in leptin receptors i.e. mice that supposedly didn’t have any effectual leptin in their bodies. Both types of mice apparently overindulged and put on weight.
The study mice were compared with normal mice to keep a record of knee osteoarthritis. The measurements apparently included pro- and anti-inflammatory cytokines present in arthritis, and a number of tests to supposedly evaluate bone changes in the knees of the mice.
Osteoarthritis was apparently not formed even though the knee bones of the leptin-free, obese mice supposedly altered. The levels of inflammatory cytokines, which apparently connect with arthritis, were seen to be mostly unaffected in these mice. The outcomes claimed that leptin may have a double role in the development of osteoarthritis by apparently adjusting both the skeletal and immune systems.
Guliak quoted, “If you are obese, there are benefits to losing weight in terms of arthritis. For example, if you are obese and lose just 10 pounds, pain decreases significantly. Pain modulation is another clue it might be a chemical or systemic metabolic effect, rather than just a mechanical effect of less weight on the joints.”
Guliak mentioned, “With obesity and osteoarthritis, there are good similarities between humans and mice. If we can find a pathway that links a high-fat diet with arthritis, then we can try to identify and block the inflammatory mediators that are linked with the dietary fat.”
Griffin is of the opinion that additional analysis and experiments need to be conducted to further understand how leptin mediates the development of osteoarthritis.
This study was published in the journal Arthritis & Rheumatism.