Review Article
Bariatric Embolization of the Gastric Arteries for the Treatment of Obesity

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Abstract

Obesity is a public health epidemic in the United States that results in significant morbidity, mortality, and cost to the health care system. Despite advancements in therapeutic options for patients receiving bariatric procedures, the number of overweight and obese individuals continues to increase. Therefore, complementary or alternative treatments to lifestyle changes and surgery are urgently needed. Embolization of the left gastric artery, or bariatric arterial embolization (BAE), has been shown to modulate body weight in animal models and early clinical studies. If successful, BAE represents a potential minimally invasive approach offered by interventional radiologists to treat obesity. The purpose of the present review is to introduce the interventional radiologist to BAE by presenting its physiologic and anatomic bases, reviewing the preclinical and clinical data, and discussing current and future investigations.

Section snippets

Rationale for BAe

The neuroendocrine functions of the gastrointestinal (GI) tract in regulating energy expenditure and metabolic homeostasis are well-known but have become the focus of scientific interest in light of the global obesity epidemic. Presently, numerous studies have confirmed that the success of bariatric surgery is not entirely related to the nutrient/volume restriction but is dependent on its profound physiologic effect (endocrine and neuronal in nature) (10, 11). In fact, one of the most dramatic

Neuroendocrine Signals between the Gi Tract and Central Nervous System

The neuroendocrine signals involved in metabolic homeostasis that arise from the GI tract can generally be categorized as long-acting or short-acting, but it should be noted that some GI-produced hormones can induce both long- and short-acting effects (13) (Table). Long-acting signals have an important role in maintaining body weight by controlling energy expenditure and fat metabolism, whereas short-acting signals typically regulate the initiation of meals via the feeling of hunger and the

PYY3-36

PYY3-36 is the bioactive form of PYY, which is released from the mucosa of the small bowel in response to ingested food (15). It is believed, but not definitively known, that PYY3-36 also induces satiety by delaying gastric emptying. Clinical studies investigating the infusion of PYY3-36 as a means to combat obesity have had variable results. For example, one study (19) found that the peripheral infusion of PYY3-36 reduced caloric intake in lean and obese patients by as much as 31%. Other

GLP-1

GLP-1 is produced by the L cells of the distal small bowel and colon in response to ingested food (15) and has been regarded as the “ileal brake” with regard to food intake. GLP-1 imparts satiety through activations of receptors in the vagus nerve, proximal GI tract, pancreas, brainstem, and hypothalamus (15). In addition, the effect of GLP-1 secretion is multifaceted, including delay of gastric emptying, increased insulin secretion, decreased gastric acid secretion, and decreased glucagon

Ghrelin: An Exciting Target for Obesity

Ghrelin is an intriguing prospective therapeutic target in the bariatric treatment population because of its potent orexigenic effects and singular role in the short- and long-acting regulation of body weight. Potential pharmacologic interventions aimed at ghrelin production or receptor binding have been previously suggested (27). First, given that ghrelin is produced from a precursor peptide called preproghrelin, one could attempt to modify or interrupt the cleavage process in an effort to

BAe: A New Approach to Treat Obesity

The stomach is classically separated into five major sections: cardia, fundus, body, antrum, and pylorus (Fig 5a). Although each section of the stomach has a unique role in the digestive process, the fundus serves as the epicenter for the neuroregulatory pathways involved with satiety and appetite stimulation (32, 33, 34). Ghrelin is expressed mainly in the fundus, which contains 10–20 times more ghrelin per gram of tissue than the duodenum, which is the next richest source (13).

Anatomically,

Current Investigations and Future Directions

Despite promising preclinical and early clinical data, there are many unanswered questions that require investigation before BAE can be routinely offered to patients undergoing bariatric treatment. For example, the complicated vascular anatomy of the stomach and its rich supply of collateral vessels creates a technical challenge to administer small particle or liquid embolic agents without nontarget embolization and resultant tissue damage in a population of patients without a terminal illness.

Conclusions

In preclinical studies, bariatric embolization appears to have a global effect on the function of the stomach. In addition to decreasing ghrelin production in the fundus, BAE also indirectly affects acid production, gastric motility, and possibly absorption. Therefore, analogous to an SG, bariatric embolization appears to impact body weight through the synergetic effects of manipulation of the hormonal and physiologic function of the stomach.

However, there is still a tremendous need to expand

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    C.R.W. received funding for this research from Merit Medical (South Jordan, Utah), Siemens (Forchheim, Germany), and the National Institutes of Health (NIH). D.L.K. received funding for this research from Siemens and NIH and has patent ownership or part ownership in imaging visible beads. A.A. received funding for this research from Siemens and Merit Medical, is a paid consultant for Surefire Medical (Westminster, Colorado), W.L. Gore & Associates (Flagstaff, Arizona), and ENDOBAR (New York, New York), and has patent ownership or part ownership in a Surefire catheter. None of the other authors have identified a conflict of interest.

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