Bariatric Artery Embolization (BAE)


Ghrelin is the hunger hormone. It is primarily produced in the stomach, specifically by cells called X/A cells that live in a portion of the stomach called the fundus. (Figure 1) Once produced, ghrelin travels through the bloodstream from the stomach to the brain and signals the brain to seek food and feel hungry.


Millions of dollars have been spent by drug companies trying to block ghrelin without success. We have, however, been successful in blocking ghrelin through gastric bypass surgery by excluding the portion of the stomach that produces ghrelin. (Figure 2) In fact, recent studies have confirmed that the reason gastric bypass patients lose weight – and even cure their diabetes and other obesity related conditions – is because hunger hormone profiles change after the surgery.



Bariatric artery embolization is a new way to shut down ghrelin producing cells. Interventional radiologists use X-ray guidance to steer a catheter into the artery that supplies the portion of the stomach that contains the ghrelin producing cells. Using small particles, the artery is blocked and the tiny ghrelin factories closed. (Figure 3) The entire procedure is performed through a tiny hole in the groin (the same method used for heart catheterizations, liver cancer embolizations, and other), nonsurgically.


In the months following the procedure patients can lose significant amounts of weight. The outcomes of BAE can be markedly improved with implementation of exercise and diet modifications during the months following the procedure – such that the effect of either interventions is accelerated by the other.



References [1-8]

  1. Weiss, C.R., et al., Bariatric Embolization of the Gastric Arteries for the Treatment of Obesity. J Vasc Interv Radiol, 2015.
  2. Borer, K.T., et al., Appetite responds to changes in meal content, whereas ghrelin, leptin, and insulin track changes in energy availability. J Clin Endocrinol Metab, 2009. 94(7): p. 2290-8.
  3. Disse, E., et al., Systemic ghrelin and reward: effect of cholinergic blockade. Physiol Behav, 2011. 102(5): p. 481-4.
  4. Karra, E., A. Yousseif, and R.L. Batterham, Mechanisms facilitating weight loss and resolution of type 2 diabetes following bariatric surgery. Trends Endocrinol Metab, 2010. 21(6): p. 337-44.
  5. Moran, T.H. and M.J. Dailey, Intestinal feedback signaling and satiety. Physiol Behav, 2011. 105(1): p. 77-81.
  6. Stensel, D., Exercise, appetite and appetite-regulating hormones: implications for food intake and weight control. Ann Nutr Metab, 2010. 57 Suppl 2: p. 36-42.
  7. Dockray, G.J., Gastrointestinal hormones and the dialogue between gut and brain. J Physiol, 2014. 592(Pt 14): p. 2927-41.
  8. Barja-Fernandez, S., et al., Peripheral signals mediate the beneficial effects of gastric surgery in obesity. Gastroenterol Res Pract, 2015. 2015: p. 560938.




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