Introduction
Obesity ranks among the most leading indicators pointing to vulnerability to a certain form of cancers, diabetes, musculoskeletal diseases, cardiovascular diseases and pulmonary diseases. The ascending tendency of obesity occurrence amongst adults caused a phenomenal rise in type 2 diabetes mellitus (T2DM). Insulin resistance and obesity are the major factors of metabolic disorder and culminate in weakened glucose metabolic rate. Various obesity prevention and treatment measures have been proposed such as pharmacotherapy, lifestyle and dietary modification and behavioral remedy. Nevertheless, out of all of them, bariatric surgery is still the most effective therapy to accomplish a continual drop in weight.
Bariatric Surgery and Diabetes Remission
Bariatric surgery is commonly linked with significant and sustained reduction of weight in very obese patients. Additionally, higher rates of long and short-term diabetes remission have been induced by this procedure. Despite the intervention of various means of controlling type 2 diabetes, bariatric surgery is still regarded as best amongst the few modalities well recognized for its remission and to prevent obese patients from acquiring diabetes. This has led to the operations such as laparoscopic adjustable gastric banding LAGB) and (RYGB) to be involved in the diabetes societies treatment guidelines such as the International Diabetes Federation and America Diabetes Association (Ali Ardestani1, 2015).The fact is bariatric surgeries result in momentous improvement in glucose homeostasis, however, most patients are on oral hypoglycemic agents.
The Effects of Bariatric Surgery upon Gut Peptides
Bariatric surgery is linked with many beneficial metabolic impacts which are attributed to profiles of altered peptide hormones, especially involving gut and the control by the influence of nervous and hormones (Meek, Lewis, Reimann, MGribble, & JPark, 2016). Various gut hormones are known for the responsibility of regulating satiety and appetite and control the gut movement thus food transit through the intestines.
Changes in Specific Gut Hormones Following Bariatric Surgery
Insulin
Bariatric surgery can cure diabetes or cause insulin remission, and this is apparently related to its capacity of improving the sensitivity of insulin and the function of the beta cell, though the exact mechanisms are wrongly understood. Bariatric surgery has some benefits to glucose and insulin homeostasis which are mediated by the loss of weight. Though all kinds of bariatric surgery can exert beneficial impacts glucose tolerance through loss of weight, certain procedures like RYGB are linked with better improvements in metabolic health compared to weight loss only. There are other procedures like gastric banding which contain more modest results on glucose and insulin which can be well explained by weight loss alone (Meek, Lewis, Reimann, MGribble, & JPark, 2016).
Ghrelin
Ghrelin is synthesized in the pancreas and the stomach during fasting and other incidents linked with hunger. The impact of bariatric surgery on ghrelin is not clear cut as different procedures give different impacts upon its secretion, mostly due to the anatomical disparities that change the contact level between the gastric fundus mucosa and ingested nutrients where the cells that produce ghrelin are located. Ghrelin levels increase with gastric banding (Meek, Lewis, Reimann, MGribble, & JPark, 2016).
Gastrin
Enteroendocrine G cells produce gastrin that preponderates within the duodenum and gastric antrum and is produced for the distension of gastric and food. Following RYGB, the levels of postprandial gastrin go, especially, in the first two weeks postoperatively (Korner, 2010). This goes on and can prolong up to one year. After the surgery, the remnant stomach undergoes various histological changes such as atrophic gastritis and chronic gastritis. In some instances, there has been a demonstration of an increased rate of proliferation in the excluded gastric antrum epithelium followed by G cells reduction. Also, there are suggestions that excessive production of gastric acid is probably involved in the abnormal histological findings pathogenesis after the surgery (Hedberg et al.2005). In clinical practice, there are many patients who start therapy of proton pump inhibitor post-operatively so as to reduce the production of gastric acid and increased gastrin and prevent complications related to acid.
Cholecystokinin (CCK)
Following bariatric surgery, stimulants of CCK release like releasing factors of intra-luminal and impulses of parasympathetic are important (Liddle, 1995). There is an explanation that the surgery can lead to an increased cholecystokinin cells stimulation in the distal small intestines or tamper with the cholecystokinin-synthesizing cells number in the duodenal mucosa which can result to a high production of CCK for a given level of stimulus (Mendieta-Zerón et al. 2011). However, CCK’s level in the bariatric surgery efficacy is not clear. Theoretically, high levels of CCK may lead to increase in satiety and improve the glucose homeostasis after RYGB. This is, however, said to result from poor responders of RYGB compared to good ones.
The importance of cholecystokinin in the ability of bariatric surgery to produce intended results is uncertain In theory increased cholecystokinin levels may result in higher repletion and better glucose breakdown after RYGB. Researchers came to realize that cholecystokinin concentrations were more pronounced in patients who achieved minimal weight loss as opposed to patients with the excellent response after surgery.
A extensive research has been taken to understand the changes in CCK taking place in the aftermath of different bariatric alternatives. One study examined respondents up to 12 months following RYGB or sleeve gastrectomy. Though the results pointed out to both groups exhibiting higher postprandial cholecystokinin degrees than the concentrations preceding operations, the sleeve gastrectomy was linked with a more so
significant cholecystokinin rise in contrast to the RYGB group. This variation was observed at one week following an operation and soared higher and higher in the course of the first year.Gastric banding influence on CCK concentrations is not well established.
GIP
The procedures of bariatric surgery such as RGYB which prevent or reduce the exposure of nutrient to the jejunum and duodenum result leads to a decrease in postprandial GIP secretion, an impact that in diabetic subjects is more pronounced (Salinari et al. 2009). After the bariatric surgery, fasting GIP reductions have also been found, though, most research reports have not described the levels of postprandial and fasting GIP. Absence or presence of diabetes may affect the altered postprandial and fast GIP responses to bariatric surgery (Laferrère et al. 2007). Bariatric surgery may lessen the levels of postprandial GIP.
GLP-1
L cells secrete Glucagon-like peptide 1 which predominates in the colon and distal ileum. After bariatric surgery, GLP-1 fasting concentrations do not change much, though, there is an evidence that suggests that the levels of postprandial increase compared to the pre-surgical states of other surgeries like RYGB, gastric banding and sleeve gastrectomy (Dirksen et al. 2013). The reasons for the increase are not established yet but are attributed to the high integral nutrients delivery to the ileum through hindgut hypothesis or anatomical alterations. The foregut hypothesis claims that the upper small intestines exclusion is accountable for bariatric surgery positivities, mostly through ‘anti-incretin’ factor reduced secretion (Rubino, 2006).
There is a wide belief that GLP-1 accounts for a significant portion of the beneficial impacts of RYGB on reduction in weight and more tolerance to glucose, however, it is still difficult to logically explain all the observed effects. It has been discovered that the essential metabolic impacts of RYG on beta-cell sensitivity were inhibited by the influx of exendin-9, a GLP-1 receptor antagonist (GLP1R) demonstrating that GLP-1 activity is of utmost importance in realizing enhanced glucose tolerance post-surgery. Some evidence also indicates that GLP-1 concentration may have a direct relationship to the successful outcome of a patient following bariatric surgery. Dirksen et al. following a research established that concentrations of GLP-1 were inflated in respondents who had undergone immense margins of weight decrease post-surgery as opposed to those who lost less weight. Nevertheless, another study showed that sleeve gastrectomy was largely influential in GLP-1 receptor experimental mice demonstrating that the GLP-1 receptor is not requisite for positive results and that additional alternative procedures are necessary. On the other hand, it is currently clear that RYGB has a positive impact on two mouse experiments in lack of enough GLP-1 and that the subsequent outcomes were at par with RYGB control mice. Hence, this is an indication that while GLP-1 participate in attenuating the benefits of bariatric surgery upon metabolism, the important role of other mechanisms should not be overlooked and GLP1R agonism does not work exclusively produce the satisfactory effect.
Conclusions
Bariatric surgery is the only treatment known that has shown a proven impact at inducing fast and sustained loss of weight with metabolic effects which are beneficial like the type 2 diabetes remission. There have been various surgical approaches which have been tested before, but the current practice focuses on RYGB, sleeve gastrectomy, and gastric banding. People still understand the effects of bariatric surgery poorly, though in etiology they are multifactorial. Bariatric surgery effect on the tolerance of glucose is likely to be associated to incretin hormone increased production, GLP-1, which contains deep insulinotropic action, linked to the sensitivity of enhanced insulin that results from weight decrease. The acute calorie restriction that happens after the surgery with beneficial hormonal milieu indorses loss of weight which, unusually, can be maintained going forward. In part, this is related to
Satiety-promoting Peptides sustained increase such as PYY3–36, GLP-1, gastrin, GIP and oxyntomodulin, and reduction in factors that promote hunger like ghrelin.
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