Treating obese mice with the cytokine known as TSLP led to significant abdominal fat and weight loss compared to controls, according to new research published Thursday in Science from researchers in the Perelman School of Medicine at the University of Pennsylvania. Unexpectedly, the fat loss was not associated with decreased food intake or faster metabolism. Instead, the researchers discovered that TSLP stimulated the immune system to release lipids through the skin’s oil-producing sebaceous glands.
The research was carried out in mice but the immunological principles should operate in humans in a quite similar fashion.
The diagram above reveals that the release of lipids is a systemic phenomenon, body-wide. You can imagine the coating of fat that would accumulate around the bodies of many of the people one sees every day, walking about. This technique might even be explored as a new source of renewable energy.
It is impossible to overstate how important it would be to find an antidote to the obesity epidemic — particularly among persons with other illnesses such as diabetes, heart disease, or arthritis of the weight-bearing joints.
To test the effect of TSLP on Type 2 diabetes, the researchers injected obese mice with a viral vector that would increase their bodies’ TSLP levels. After four weeks, the research team found that TSLP had not only affected their diabetes risk, but it had actually reversed the obesity in the mice, which were fed a high-fat diet. While the control group continued to gain weight, the weight of the TSLP-treated mice went from 45 grams down to a healthy 25 grams, on average, in just 28 days.
Most strikingly, the TSLP-treated mice also decreased their visceral fat mass. Visceral fat is the white fat that is stored in the abdomen around major organs, which can increase diabetes, heart disease, and stroke risk. These mice also experienced improved blood glucose and fasting insulin levels, as well as decreased risk of fatty liver disease.
Given the dramatic results, Kambayashi assumed that the TSLP was sickening the mice and reducing their appetites. However, after further testing, his group found that the TSLP-treated mice were actually eating 20 to 30 percent more, had similar energy expenditures, base metabolic rates, and activity levels, when compared to their non-treated counterparts.
To explain the weight loss, Kambayashi recalled a small observation he had previously ignored: “When I looked at the coats of the TSLP-treated mice, I noticed that they glistened in the light. I always knew exactly which mice had been treated, because they were so much shinier than the others,” he said.U Penn Medicine
Manipulation of the immune system in this manner has always been a likely therapeutic destination, eventually. Such approaches to therapeutics have important implications not only for basic health, but also for longevity.
Scientists are just beginning to untangle the relationships between obesity and dysfunctional immune processes:
Obesity, like other states of malnutrition, is known to impair the immune function, altering leucocyte counts as well as cell-mediated immune responses. In addition, evidence has arisen that an altered immune function contributes to the pathogenesis of obesity. This review attempts to briefly comment on the various plausible explanations that have been proposed for the phenomenon: (1) the obesity-associated increase in the production of leptin (pro-inflammatory) and the reduction in adiponectin (anti-inflammatory) seem to affect the activation of immune cells; (2) NEFA can induce inflammation through various mechanisms (such as modulation of adipokine production or activation of Toll-like receptors); (3) nutrient excess and adipocyte expansion trigger endoplasmic reticulum stress; and (4) hypoxia occurring in hypertrophied adipose tissue stimulates the expression of inflammatory genes and activates immune cells. Interestingly, data suggest a greater impact of visceral adipose tissue and central obesity, rather than total body fat, on the inflammatory process. In summary, there is a positive feedback loop between local inflammation in adipose tissue and altered immune response in obesity, both contributing to the development of related metabolic complications.
If humans can keep the vultures from completely taking over global economies and societies, we will eventually approach the state where health, fitness, and longevity are almost entirely matters of personal choice.
Hope for the best. Prepare for the worst. It is never too late to have a Dangerous Childhood © .