Researchers begin to map the control of body fat by the brain.


By uncovering the action of two naturally occurring hormones, scientists may have discovered a way to assist in the shedding of excess fat.  The findings from Monash University researchers give new insights into how the brain regulates body fat and may lead to more effective ways to lose weight and prevent obesity by promoting the conversion of white fat to brown fat. The opensource study is published in the journal Cell.

The team unravelled a molecular mechanism that depends on the combined action of two hormones, leptin, an appetite suppressant generated in fat cells, and insulin, produced in the pancreas in response to rising levels of glucose in the blood. Their research shows that the two hormones act in concert on a group of neurons in the brain to stimulate the burning of body fat via the nervous system.

The team state that discovering the combined action of these two hormones makes could assist in the shedding of excess fat.  It is known that these hormones give the brain a comprehensive picture of the fatness of the body. Because leptin is produced by fat cells, it measures the level of existing fat reserves, the more fat, the more leptin. Whereas insulin provides a measure of future fat reserves because glucose levels rise when we eat.

Fat in adult humans is typically stored in adipocytes, specialised cells that comprise white fat. But around the neck and shoulders, there is a second form of fat made of brown adipocytes. Rather than storing fat, these cells can be induced to burn it off.

The research team discovered leptin and insulin interact with proopiomelanocortin (POMC) neurons in the brain’s hypothalamus, causing them to send signals through the nervous system promoting the conversion of white fat into brown fat. This leads to burning off of excess fat.

The researchers were able to show that the process is regulated in these neurons by enzymes known as phosphatases, which inhibit the actions of each of the hormones. When the levels of these inhibitors were reduced, the browning and burning of fat increased.

The team state that this fundamental process normally serves to maintain body weight but in diet-induced obesity this mechanism goes awry.  Eventually, the researchers state that they may be able to help people lose weight by targeting these two enzymes. Turning white fat into brown fat is a very exciting new approach to developing weight loss agents going to the body’s main regulator, the brain, to achieve this.

Source:  Monash University

The primary task of white adipose tissue (WAT) is the storage of lipids. However, “beige” adipocytes also exist in WAT. Beige adipocytes burn fat and dissipate the energy as heat, but their abundance is diminished in obesity. Stimulating beige adipocyte development, or WAT browning, increases energy expenditure and holds potential for combating metabolic disease and obesity. Here, we report that insulin and leptin act together on hypothalamic neurons to promote WAT browning and weight loss. Deletion of the phosphatases PTP1B and TCPTP enhanced insulin and leptin signaling in proopiomelanocortin neurons and prevented diet-induced obesity by increasing WAT browning and energy expenditure. The coinfusion of insulin plus leptin into the CNS or the activation of proopiomelanocortin neurons also increased WAT browning and decreased adiposity. Our findings identify a homeostatic mechanism for coordinating the status of energy stores, as relayed by insulin and leptin, with the central control of WAT browning.  Leptin and Insulin Act on POMC Neurons to Promote the Browning of White Fat.  Tiganis et al 2015.

The primary task of white adipose tissue (WAT) is the storage of lipids. However, “beige” adipocytes also exist in WAT. Beige adipocytes burn fat and dissipate the energy as heat, but their abundance is diminished in obesity. Stimulating beige adipocyte development, or WAT browning, increases energy expenditure and holds potential for combating metabolic disease and obesity. Here, we report that insulin and leptin act together on hypothalamic neurons to promote WAT browning and weight loss. Deletion of the phosphatases PTP1B and TCPTP enhanced insulin and leptin signaling in proopiomelanocortin neurons and prevented diet-induced obesity by increasing WAT browning and energy expenditure. The coinfusion of insulin plus leptin into the CNS or the activation of proopiomelanocortin neurons also increased WAT browning and decreased adiposity. Our findings identify a homeostatic mechanism for coordinating the status of energy stores, as relayed by insulin and leptin, with the central control of WAT browning. Leptin and Insulin Act on POMC Neurons to Promote the Browning of White Fat. Tiganis et al 2015.

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