We examined the effects of two types of weight loss surgery on changes in body composition and systemic metabolism in a small group of women. At 24 months, significant differences between the two groups were found. Although both Roux-en-Y and gastric banding patients showed significant improvement in many measured parameters, Roux-en-Y patients reached a plateau while banding patients began to rebound. A progressive return of metabolic markers of obesity was seen in gastric banding patients but not in Roux-en-Y patients.
The discrepancy in results between the two cohorts suggests that the mechanisms of weight loss differ between Roux-en-Y gastric bypass surgery and gastric banding. While both Roux-en-Y gastric bypass and gastric banding have a restrictive component, recent evidence suggests that bypass of the upper intestine in the Roux en Y procedure may lead to greater weight loss through an alteration of hormone levels and other factors within the satiety crosstalk between the gut and the brain.11,12
Furthermore, the radical changes in satiety and adipose tissue derived hormone levels that occur after a Roux-en-Y procedure may sustain long term weight loss and prevent weight rebound to a greater degree than the obvious restrictive and malabsorptive nature of the surgery would predict.11,12
Others have shown that weight loss leads to improved insulin sensitivity.13,14
There is also evidence that a Roux-en-Y gastric bypass results in greater improvement in insulin resistance by bypassing the hormonally active foregut.15
In our study, Roux-en-Y patients at 24 months had significantly less fat mass than their gastric banding counterparts (28.9 kg as opposed to 45.7 kg). Yet, it is the metabolically active components of fat, the adipocytes, which are likely to play a vital role in explaining the disparity in weight loss between Roux-en-Y and gastric banding patients. Adipocytes produce many bioactive peptides, such as leptin and adiponectin, that have been shown to modulate insulin responsiveness.16
In our study, Roux-en-Y patients had significantly lower leptin levels than banding patients (13.2 ng/mL as opposed to 52.6 ng/mL, respectively). In the Roux-en-Y cohort, leptin also correlated significantly with weight, fat mass, insulin, and HOMA. () These findings are similar to results by Infanger et al.
who found that leptin levels correlated linearly with fat mass in patients who underwent weight loss surgery when compared with overweight fat mass in matched controls two years after surgery.17
These findings also suggest that leptin not only decreases with loss of weight and fat mass, but also modulates insulin resistance. In this context it is of interest that leptin receptors are expressed on pancreatic β-islet cells and leptin inhibits insulin secretion and transcription of the preproinsulin gene.18,19
Studies in mice have demonstrated that administration of leptin to either normal, obese, or diabetic animals improves insulin sensitivity and reduces hyperinsulinemia.20
Other studies have pointed to the release of factors from the duodenum and proximal foregut in response to food stimulation that may be responsible for some degree of “leptin resistance” and the corresponding elevated leptin levels observed in obese patients.21
Putting all of this together, our data suggest a change in leptin resistance that is associated with weight loss which appears to be more pronounced in the Roux-en-Y cohort.
Circulating adiponectin levels are also potent regulators of insulin sensitivity.22,23
Recent studies have indicated that by changing the activity of modulators of the insulin signaling pathway, such as 5′ AMP-activated kinase, adiponectin can improve both beta cell function and insulin secretion.24,25
After 24 months, significant correlations between adiponectin and both serum insulin and HOMA were found in our Roux-en-Y patients. Our findings are consistent with those reported by Guldstrand and colleagues who measured beta cell function and insulin resistance in obese patients. Their study found a linear correlation (r = 0.46, p = 0.012) between the increase in plasma adiponectin levels and insulin sensitivity in patients who underwent weight loss surgery.26
The partial reversal in many anthropometric parameters, measures of insulin sensitivity, and adipokines at two years in our gastric banding patients is disturbing. In a five year prospective randomized trial, Angrisani and colleagues compared the outcomes of both Roux-en-Y and gastric banding patients.27
The percentage of weight loss failure (as defined by BMI >35 kg/m2
at 5 years) was 34.6% in banding patients as opposed to 4.2% in bypass patients (p < 0.001). The BMI at only 2 years after surgery of our gastric banding patients is 36.3 kg/m2
(BMI of 44.9 kg/m2
at baseline). The large discrepancy in percent weight loss for our patients after twenty four months (37.4% for Roux-en-Y patients; 19.5% for gastric banding patients) is consistent with other studies comparing the two patient cohorts.28,29
Beyond the anthropometric values, our gastric banding patients show increases in serum glucose levels, insulin levels, and HOMA between nine and twenty four months that did not reach statistical significance.
Also observed in this group was the partial reversal in adipokines (such as leptin and hs-CRP), LDL, and total serum cholesterol. While these trends were not significant, they suggest that further research with larger numbers of patients is required. Sjostrom et al.
from the Swedish Obesity Study show that gastric banding patients had a higher BMI, glucose, and insulin than the gastric bypass patients.30
In their study, adipokines were not measured. In light of the role of adipokines in insulin resistance, further research is needed to better understand the mechanism of weight loss beyond caloric restriction and malabsorption that accompanies a Roux-en-Y procedure.