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Research program 2 – Obesity gravitostat

The gravitostat: A body weight homeostat that regulates body fat mass.

 
In an additional line of research, Professor Jansson collaborate with Professor Claes Ohlsson at Institute of Medicine at Sahlgrenska Academy to tease out a novel mechanism for homeostatic regulation of body weight . The data obtained in this project imply the existence of internal bathroom scales in the body. We believe that the weight of the body is registered in the lower extremities. If the body weight tends to increase, a signal may be sent to the brain to decrease food intake and keep the body weight constant. This homeostatic regulation of body weight is called the gravitostat.


Studies have been performed on obese rodents that were made artificially heavier by loading with extra weights. The animals then lose almost as much weight as the artificial load. The extra weights caused body fat to decrease and blood glucose levels to improve (Jansson JO et al, 2018)(Ohlsson & Jansson, 2018, 1)(Ohlsson & Jansson, 2018, 2). Before our study, the only known homeostatic regulator of fat mass was the fat-derived hormone leptin discovered by Friedman almost a quarter of a century ago (Zhang Y et al, 1995).

 

Fig 1. The gravitostat body weight sensor is leptin independent. Chronical static loading (High Load) suppresses body weight in leptin deficient Ob/Ob mice. The control mice are Ob/Ob mice with Low Load (empty capsule).

 

 Importantly, the gravitostat regulates fat mass independently of fat-derived leptin, as indicated by the fact that loading can suppress body weight in ob/Ob mice that have no leptin (See Fig 1). This finding show there are two independent homeostatic systems for fat mass regulation.
Very recently, we have presented evidence that the gravitostat regulates fat mass in obese mice while leptin regulates fat mass only in lean mice with low endogenous serum leptin levels. We propose that activation of the gravitostat primarily protects against obesity while low levels of leptin protects against undernutrition (Ohlsson C et al 2018).
Lately, several studies of human populations have coupled sitting with obesity and obesity related diseases (Levine JA et al, 2005). The present results from Jansson´s and Ohlsson’s labs could explain why. The gravitostat sensor gives an inaccurately low measure when people sit down. As a result people may eat more and gain weight.

 

 Fig 2. Hypothesis for homeostatic regulation of body fat mass by two different signal systems. The first previously known pathway is fat derived leptin in circulation acting on the brain to decrease food intake and fat mass. The second, novel, mechanism is that increased fat mass is counteracted by the body weight homeostat (“gravitostat”). Increased body weight activates a sensor dependent on the osteocytes of the weight bearing bones. This induces an afferent signal to reduce food intake (Jansson JO et al 2018).




 

Page Manager: Annie Sundling|Last update: 9/26/2018
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Denna text är utskriven från följande webbsida:
http://neurophys.gu.se/english/departments/physiology/research/endocrinology/john-olov-jansson/research-program-2/
Utskriftsdatum: 2019-11-20