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|This table offers a comprehensive summary
illustration of how many cardiometabolic risk factors may be affected by the
ECS. In the brain, the hypothalamus receives and integrates signals
regarding the status of body-fat stores from adipose tissue and other
peripheral tissues. CB1-R overactivity in the hypothalamus is associated
with excess adiposity. CB1-R activation in the hypothalamus also sustains
overeating in obese animals. Endocannabinoids have been documented in
adipose tissue, with CB1-R having been shown to be active in stimulating
lipogenesis. Ongoing investigation in animals indicates that, in skeletal
muscle, CB1-R stimulation reduces insulin-mediated glucose uptake. In the
liver, it has been demonstrated that endocannabinoid-mediated increase in de
novo lipogenesis in the liver is a critical component in diet-induced
obesity. In the gastrointestinal tract, it is known that CB1-R activation by
anandamide increases food intake. A surge in intestinal anandamide levels
serves as a short-range hunger signal to promote feeding.
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