The neurohormonal regulation of energy intake in relation to bariatric surgery for obesity

Abstract

Obesity has reached pandemic proportions, with bariatric surgery representing the only currently available treatment demonstrating long-term effectiveness. Over 200,000 bariatric procedures are performed each year in the US alone. Given the reliable and singular success of bariatric procedures, increased attention is being paid to identifying the accompanying neurohormonal changes that may contribute to the resulting decrease in energy intake. Numerous investigations of postsurgical changes in gut peptides have been conducted, suggesting greater alterations in endocrine function in combination restrictive and malabsorptive procedures (e.g., Roux-en-Y gastric bypass) as compared to purely restrictive procedures (e.g., gastric banding), which may contribute to the increased effectiveness of combination procedures. However, very few studies have been performed and relatively little is known about changes in neural activation that may result from bariatric procedures, which likely interact with changes in gut peptides to influence postsurgical caloric intake. This review provides a background in the neurohormonal regulation of energy intake and discusses how differing forms of bariatric surgery may affect the neurohormonal network, with emphasis on Roux-en-Y gastric bypass, the most commonly performed procedure worldwide. The paper represents an invited review by a symposium, award winner or keynote speaker at the Society for the Study of Ingestive Behavior [SSIB] Annual Meeting in Portland, July 2009.

Fig. 1

Cartoon representation of the relevant influences on energy intake. The strength of evidence in support of each association is represented by the thickness of the connecting arrows with bolded lines representing strong empirical support and the dotted lines representing more theoretical evidence.

Fig. 2

Illustrations of restrictive procedures and Roux-en-Y gastric bypass. Reproduced with permission from Dr. Edward C Mun [171] A. Vertical banded gastroplasty; B. Adjustable gastric banding; C. Roux-en-Y gastric bypass.

Fig. 3

Illustrations of malabsorptive procedures. Reproduced with permission from Dr. Edward C Mun [171] A. Jejunoileal bypass; B. Biliopancreatic diversion; C. Biliopancreatic diversion with duodenal switch.

Fig. 4

Glass brain figure depicting brain activation in response to high-calorie relative to low-calorie food stimuli (high-calorie–low-calorie contrast) at p < 0.05 uncorrected. A greater difference between mesolimbic dopaminergic pathway activation in response to high-calorie foods and mesolimbic dopaminergic pathway activation in response to low-calorie foods can be seen pre-relative to post-surgery. For display purposes, activation maps are shown without a cluster extent threshold.

Fig. 5

Coronal and sagittal slices depicting areas in which the difference between activation in response to high- and low-ED foods (High-ED–Low-ED Contrast) was greater pre-relative to post-surgery. Activation was considered significant at p < 0.05 uncorrected, with an applied cluster extent threshold (k=22). The largest clusters (k>80) were seen in the dlPFC (y=42; top and cluster), ventrolateral PFC (vlPFC; y =42; bottom cluster), ventral striatum (y=4; bottom two clusters), putamen and lentiform nucleus (y =0; bottom cluster), and dmPFC (x=4; rightmost cluster). A nonsignificant cluster (k=20) was also observed in the VTA (x=4; white arrow). MNI coordinates are given in upper left corner of each panel. The color bar represents t values.

Fig. 6

The difference between the desire to eat following exposure to high-calorie relative to low-calorie foods (high-calorie–low-calorie) pre-surgery was greater than the nonsignificant high-calorie–low-calorie difference post-surgery p = 0.007; *p<0.05; **p<0.01.