Theoretic Hormonal Impact of Laparoscopic Gastric Band Surgery
Laparoscopic adjustable gastric banding, also known as the Lap-Band, is categorized as a purely restrictive procedure, yet is associated with increased fasting and postprandial satiation alongside changes to eating behavior that may not be fully accounted for by mechanical restriction of food intake alone. Whilst the majority of research into the endocrine effects of bariatric surgery has focused on malabsorbtive procedures such as the Roux-en-Y gastric bypass (RYGB), there is some evidence to support laparoscopic adjustable gastric banding exerting a direct effect upon various hormonal parameters, warranting further investigation in this area.
How Might Gut Hormones Change after Gastric Banding?
Glucagon-Like Peptide-1 and Peptide YY
A number of hormones, including glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) are produced in the gut. In addition to mediating hunger and satiety, they are also involved in modulating insulin secretion by the pancreas.
GLP-1 and PPY are produced by the L cells of the distal gut, with secretion triggered by absorption of nutrients from the intestinal tract, typically within 15 to 30 minutes after initiation of food intake. Their regulatory effects upon appetite are thought to involve several different mechanisms, including increased insulin release, reduced gastric acid secretion and delayed speed of gastric emptying.
Postprandial levels of GLP-1 and PYY are typically reduced in obese individuals, lending support to the theory that impairment of hormonally regulated satiety signals can promote increased food consumption. The influence of these hormones upon surgically induced weight loss is unclear. Whilst postprandial levels of GLP-1 and PYY appear to increase following RYGB, comparative studies of RYGB and laparoscopic adjustable gastric banding have reported unchanged levels of GLP-1 and a reduced PPY response following laparoscopic adjustable gastric banding.
The peptide hormone ghrelin is predominantly secreted by the gastric fundus, but also by other sections of gastrointestinal tract, the kidneys, hypothalamus and pituitary gland. It is involved in stimulation of appetite, influencing food intake, chewing time, taste preferences and food perception. Ghrelin is known to increase gastrointestinal motility, decrease insulin secretion and is also involved in stimulating growth hormone, cortisol and adrenaline.
Plasma ghrelin levels are largely regulated by food intake, peaking immediately prior to a meal and dropping rapidly after eating is initiated. A negative association exists between ghrelin and BMI, with obese individuals typically exhibiting reduced ghrelin levels. Increased ghrelin secretion has been reported in individuals who have undergone diet-induced weight loss, suggesting that the hormone may be implicated in long-term regulation of body weight and could contribute to the difficulties experienced by many individuals in achieving sustained weight loss through dietary interventions alone. However, the role of ghrelin in dietary and surgical weight loss has yet to be adequately defined and many confounding reports exist within the literature.
The laparoscopic adjustable gastric banding procedure is effective in promoting sustained weight loss, and is known to increase satiety and reduce hunger, yet there is also evidence to suggest that postoperative fundal ghrelin production and plasma ghrelin levels increase at a rate comparable to those observed following dietary- induced weight loss, potentially implying that changes in ghrelin following laparoscopic adjustable gastric banding occur as a result of weight loss, rather than restriction of nutrients or some other aspect of the procedure. However, other studies have reported reduced or unchanged levels of ghrelin following laparoscopic adjustable gastric banding, and it is additionally acknowledged that adjustments in band pressure can affect satiety. If ghrelin is directly implicated in laparoscopic adjustable gastric banding-induced weight loss and associated changes in appetite, its role is therefore likely to be complex, potentially involving as-yet uncharacterized prandial and postprandial effects, and possibly influenced by specific placement and pressure of the band around the gastric fundus.
Pancreatic polypeptide (PP) is a hormone closely related to PYY, secreted by the PP cells of the pancreas. It serves to regulate pancreatic hormone secretion, and is also associated with modulation of appetite and food intake. Like PYY, PP secretion is triggered by intake of food, with release governed by efferent vagal nerve activity in addition to gastrointestinal responses to nutrient intake. There is some evidence to suggest that PP meal response may be predictive of laparoscopic adjustable gastric banding-induced weight loss, with low response associated with higher weight loss.
Resection of the vagus nerve, which runs along the proximal stomach, is thought to induce weight loss, and it is therefore possible that additional pressure exerted upon the vagus nerve after food intake as a result of gastric band placement is responsible for changes in appetite and food intake observed following laparoscopic adjustable gastric banding. However, studies of PP meal response under various other conditions have reported conflicting results in terms of the relationship between PP levels and weight loss or gain.
Insulin is produced by the beta cells of the pancreas and is responsible for regulating glucose uptake and inhibiting glucagon release. Lack of or impaired sensitivity to insulin can lead to diabetes.
Whilst laparoscopic adjustable gastric banding is associated with significant improvements in insulin sensitivity and type 2 diabetes, these are typically smaller than those associated with gastric bypass surgery and tend to occur gradually, in parallel with changes in BMI. Thus they may be presumed to occur as a result of decreased caloric intake and weight loss rather than as a direct result of gastric banding. Some studies have reported improvements in glucose homeostasis within one or two days of laparoscopic adjustable gastric banding, but this is most likely attributable to short-term factors such as difficulty swallowing, that can dramatically limit food intake in the immediate postoperative period, resulting in reduced levels of glucose.
The protein hormone leptin is predominantly secreted by adipose tissue. Implicated in regulation of body weight and metabolism, it is known to suppress appetite, and is also associated with insulin resistance due to its inhibitory effects upon glucose-stimulated insulin production.
Obese individuals typically exhibit high circulating levels of leptin, proportional to adipose tissue mass. Prolonged exposure to high concentrations of leptin is thought to cause desensitization or leptin resistance, such that it fails to effectively promote satiety in obese individuals. Conversely, dietary or surgically induced weight loss typically precipitates restoration of normal leptin levels. Reports in the literature vary, but the majority of findings suggest that leptin levels appear to reduce proportionally to BMI following laparoscopic adjustable gastric banding, suggesting that weight loss rather than any direct effects of surgery are responsible.
Adiponectin is an anti-inflammatory protein hormone secreted exclusively by adipose tissue, at levels inversely correlated with BMI, such that obesity is associated with reduced adiponectin expression. It is involved in promotion of glucose uptake, can improve insulin sensitivity and is negatively associated with development of insulin resistance and type 2 diabetes.
Weight loss induced by diet or surgery is known to result in increased adiponectin secretion, and there is also evidence to suggest that adiponectin levels persistently increase following laparoscopic adjustable gastric banding, independently of BMI reduction. One possible explanation for this effect is that visceral fat may exert greater influence on adiponectin levels than subcutaneous fat, and correlation between BMI and visceral fat mass is thought to be low when compared to other measures such as waist-to-hip ratio and waist circumference. Mode of weight loss is known to impact upon adiponectin levels, with exercise-induced weight loss not associated with altered adiponectin levels, even when improved insulin sensitivity and decreased abdominal adiposity occur. It is therefore possible that laparoscopic adjustable gastric banding affects adiponectin levels independently of weight loss via some as-yet unidentified mechanism, but further research in this area is required.
Obesity is associated with impaired fertility and sexual function in males. Obese men typically exhibit elevated levels of estrogen, and reduced levels of testosterone, luteinizing hormone (LH) and follicle stimulating hormone (FSH). Estrogen is produced by adipose tissue, and can suppress LH, which is required for stimulation of testosterone production within the testes. Thus, testosterone levels are negatively correlated with BMI. Obesity-related disruption of male reproductive hormones can lead to various fertility issues including erectile dysfunction and reduced sperm quality.
The available evidence is supportive of weight loss achieved via diet or surgical intervention leading to a general improvement in male hormonal profile. However, the specific effects of laparoscopic adjustable gastric banding upon male fertility have yet to be elucidated.
Obesity is a known risk factor for ovulatory dysfunction and female infertility. Polycystic ovarian syndrome (PCOS), as characterized by anovulation in the presence of elevated testosterone levels and/or enlarged ovaries covered in multiple small cysts, is strongly associated with obesity and insulin resistance.
Significant weight loss, as facilitated by bariatric surgery, normalizes levels of testosterone and insulin, frequently leading to resolution of anovulatory infertility and improved pregnancy outcomes in premenopausal women. It is not known whether laparoscopic adjustable gastric banding differs from other procedures in terms of its effects upon female reproductive hormones.