Cannabinoid Physiology: Influence on Metabolism and Body Fat Regulation

There is accumulating scientific evidence that theendocannabinoid system plays an important role in how the body regulates energy (calorie) balance, as well as carbohydrate and fat metabolism. As such, the endocannabinoid system (ECS) is an oft-overlooked key in the regulation of body weight and body composition (note: “body composition” here refers to the relative amounts of lean mass and body fat).

Scientists have uncovered that endo/phytocannabinoids act via central (brain) and peripheral (gut, liver, muscle and fat) mechanisms. Central control of appetite, satiety, cravings, and food-seeking behavior involves a complex interplay between various centers of the brain. Different areas of the brain receive information in the form of nutrients, hormones, and signaling molecules from body fat tissue, the gut, blood, and peripheral sensory receptors.

It is accepted that endocannabinoids and certain naturally occurring phytocannabinoids in cannabis activate cannabinoid receptors type 1 and type 2 (CB1 and CB2 receptors), in addition to various other G-protein coupled receptor families (e.g., TRPV1, GPR55 and others). The CB1 receptor is believed to be responsible for most of the central effects of cannabinoids on hunger/satiety centers of the brain that affects appetite and energy intake.

Moreover, CB1 receptors have also been discovered to exist in the peripheral tissues outside of the brain, including key organs such as adipose (fat), liver, gut, pancreas, and skeletal muscle. The interplay of these central and peripheral mechanisms and their effects on body weight and body composition is currently under intense scrutiny.

Interestingly, over-activation of the endocannabinoid system, primarily via CB1 activation, has been suggested to contribute to increased abdominal obesity, glucose uptake into adipocytes (fat cells), and insulin resistance in muscle. This “metabolic dysfunction” sets up a vicious cycle whereby further insulin resistance in muscle and liver increases abdominal obesity and further CB1 over-activation, resulting in greater food-seeking behavior and increased appetite.

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