Changes in appetite are reported within days following bariatric surgery. Increased satiety and decreased hunger postoperatively have been reported after the RYGB, VSG and LAGB [16–18]. This is very much in contrast with the reports of patients who consume similar amounts of calories through dieting and describe increases in hunger, decreases in satiation and preoccupation with food (e.g. [19, 20]). This observation suggests that bariatric surgery procedures have an advantageous effect on the control of food intake, in that through changes in physiology they assist the individual reduce their caloric intake and weight loss and maintain them in the long term.

Chronic caloric deprivation is normally accompanied by a decrease in resting energy expenditure as the body strives to conserve energy [42]. These are some inconsistencies as to what happens to resting energy expenditure after bariatric surgery, but the majority of human and/or animal studies have shown that it remains stable on decreases after RYGB, VSG and AGB [21, 43–52]. However, a more consistent finding from both humans and rodents is that postprandial energy expenditure is higher after RYGB compared to controls [53–55]. Similar experiments have not been performed after VSG or AGB.

The postprandial energy expenditure increases after RYGB are mechanistically intriguing. Gut hormones may contribute to enhanced postprandial thermogenesis through centrally mediated sympathetic nervous system activation. Against this hypothesis, acute peripheral administration of exendin (9–39), a GLP-1 receptor antagonist did not alter energy expenditure in rodent models of RYGB [56]. An alternative hypothesis is that the elevation in the plasma levels of bile acids after RYGB may lead to heightened activation brown adipose tissue and consequently higher postprandial thermogenesis. Unfortunately, the only available rodent study failed to demonstrate this [57]. Therefore the mediators underlying this paradoxical increase in energy expenditure in the context of weight loss remain elusive, but have attracted considerable interest as they may be the targets of novel anti-obesity pharmacotherapy.

The role of gut microbiota in the context of obesity and weight loss has attracted significant interest. Obesity is associated in some, but not all studies, with an unfavourable colonisation of the bowel with bacteria that are more efficient in extracting energy from nutrients and storing it as fat [58]. A profound disturbance of this colonisation has been observed after RYGB in particular and includes the reduction in Prevotellaceae, Archea, Firmicutes, Bacteroidetes and an increase in the Bacteroidetes/Prevotella ratio and Gammaproteobacteria [59–61]. These alterations may be due to weight loss itself, changes in macronutrient proportions in the diet, anatomical manipulations, pH and bile flow amongst others. The confounding effects of variations in these factors together with the antibiotic use and metabolic control may be the cause of the variability of the results in the handful of published studies. More recently, other novel mediators that may contribute to weight loss have surfaced. In a series of very elegant experiments, the transfer of gut microbiota from mice that have undergone RYGB to germ-free mice lead to 5 % weight loss in the latter group, potentially through altered short-chain fatty acid production and signalling [62].

A number of human studies have reported that it is not only total caloric intake that is lower after RYGB, but also the percentage of calories from fat and sugar as compared to preoperatively or after other bariatric surgical techniques such as the vertical/horizontal banded gastroplasties [43, 63–69]. Similar to the energy expenditure observation, this finding is somewhat paradoxical considering that diet-induced weight loss is normally associated with more “cravings” for high-calorie, energy dense, fatty and sweet foods in the majority of cases (e.g. [20]). The human literature does suffer from some inconsistencies as to the magnitude and durability of this observation. Indeed, the study of human eating behaviour is notoriously difficult due to the variability of human nature itself and the imprecise methods of assessing it, which is further amplified by the stigma and underreporting of caloric intake associated with obesity. Nevertheless, the caveats of human eating behaviour research can be largely avoided through the use of animal models of RYGB. The relative consumption of fat and sugar is lower in rodents after RYGB compared to sham-operated rats, a finding consistent amongst different laboratories and with the majority of the human literature (e.g. [70, 71]).

The mechanisms responsible for this “healthy” shift in food preferences have attracted considerable interest in the last few years. The available literature suggests that the mechanism is multifactorial; patients after RYGB exhibit increased taste acuity for sweets [72], the appetitive reward value of fat/sweet taste is decreased [73] and in brain reward system activation in response to food and/or high-calorie food pictures, as assessed by functional neuroimaging, is lower after RYGB compared to preoperatively or after AGB (e.g. [74, 75]). These responses may be further amplified by unpleasant post-ingestive effects of energy dense food, in the form of the dumping syndrome and condition taste aversion (e.g. [70]). VSG is also associated with similar responses to food in rodent models of the procedure [76]. The mediators underlying the lower consumption of fat and sugar after RYGB and VSG have not been elucidated yet, but may include the action of gut hormones on taste afferents and the mesolimbic brain reward system, and altered nutrient sensing and vagal signalling in the gut.

Out of all the comorbidities associated with obesity, bariatric surgery is particularly effective in improving glycaemic control in patients with T2DM. A substantial proportion of these patients achieve euglycaemia, or even normoglycaemia, in the absence of active glucose-lowering pharmacotherapy [3–6]. The high rates of glycaemic “remission” after bariatric surgery have led to the adoption of the term “metabolic surgery” to describe its potent metabolic efficacy. In the absence of a consistent definition, a high-profile meta-analysis reported remission rates of 78 % of patients after surgery [77]. Subsequent analyses of different cohorts have shown that the remission rates are 34–41 % when the more stringent glycaemic criteria of the American Diabetes Association are applied [4, 78]. Recognising the need for more holistic outcomes, the International Diabetes Federation (IDF) introduced their own criteria of optimisation of the metabolic state which incorporate markers of glycaemia, but also weight loss, plasma lipids, rates of hypoglycaemia, blood pressure control and use of medications [79]. Using these criteria in a small cohort, remission rates of only 8–14 % were achieved 1–2 years after metabolic surgery, suggesting that surgery may be better used together with, and not instead of, lifestyle modification and pharmacological treatments for T2DM for optimal metabolic outcomes [80]. Independently of what criteria are used to define metabolic remission, the clinical efficacy of metabolic remains substantial and superior to currently available best medical care. This has now been consistently proven by four RCTs [3–6] and a number of others are ongoing.

Glycaemic improvements after surgery do not follow the same pattern after all metabolic procedures. The BPD, RYGB and VSG cause rapid reductions in blood glucose within days after surgery and before significant weight loss has been achieved, in contrast to the AGB after which the reductions are slower and gradual [81–83]. As the criteria used to define T2DM remission, change from study to study, it is very difficult to make definitive conclusions on the relative efficacy of each procedure. However, the available evidence suggest that BPD is superior to RYGB and VSG, with the latter two having very similar success rates in the medium term, followed by the AGB [3–5]. These results remain the same even when patients in each surgical group are matched for weight loss, suggesting that some of these procedures have weight-loss-independent effects [3, 25]. In this section, we discuss the mechanisms underlying the observations of these RCTs. These are also summarised in Table 10.1.

After RYGB, first phase and early insulin release is increased both early postoperatively and late after significant weight loss. This is supported by the vast majority (e.g. [34, 84–98]), but not all [99], of the studies that used oral glucose/mixed meal tolerance or intravenous tests. These have shown that both the glucose and insulin responses after an oral challenge are shifted to the left, as the result of faster glucose absorption and exaggerated and rapid insulin secretion. Indeed, after RYGB, the disposition index, acute insulin response to glucose and the insulinogenic index increase in patients with T2DM, but remain stable or may even be reduced in subjects with normal glucose tolerance [94, 95, 97, 98]. Additionally, both the beta-cell sensitivity is increased and the proinsulin/insulin ratio decreases after RYGB [84, 96, 100]. As would be expected in response to weight loss and improvements in peripheral insulin resistance, the decline in insulin release after a meal is rapid, and the total postprandial area under the curve (AUC) for insulin is lower compared to preoperatively [86, 88, 89, 91, 101]. When patients after RYGB and AGB are studied following 20 % weight loss, total postprandial AUC is reduced similarly by these procedures [102]. However, the insulin curves look very different, with a characteristic earlier and greater insulin peak after RYGB, but not AGB [102]. The responses after VSG are similar to those observed after RYGB (e.g. [28, 103, 104]). The BPD is unique in that it profoundly reduces both hepatic and peripheral insulin resistance very early after surgery and before significant weight loss has taken place, but also increases early insulin secretion in patients with T2DM, but not normoglycaemic patients (e.g. [105, 106]). Again following weight loss after BPD, total postprandial AUC is substantially decreased compared to preoperatively [107].

The mechanism underlying the increased early postprandial release of insulin after RYGB is in part due to the rapid and exaggerated rise in the incretin hormone GLP-1, as administration of the GLP-1 receptor antagonist exendin (9–39) attenuates this response [108]. Whilst such mechanistic studies have not been performed after BPD, similar results to RYGB are observed after VSG in animal models [109].

There is however another side to the reversal of beta-cell dysfunction after RYGB and this is postprandial hyperinsulinaemic hypoglycaemia. In the largest patient cohort even examined through a national registry in Sweden, the relative risk of hypoglycaemia was two- to sevenfold higher after RYGB, but not VBG or AGB, compared to the general population [110]. However, the absolute rates of symptomatic hypoglycaemia remain low at 0.2–1 %.

There is controversy as to the mechanism underlying this phenomenon with some studies suggesting it is the result of beta-cell hyperplasia (e.g. [111]), whereas others supporting that it is due to “extreme” restoration of beta-cell function and GLP-1 release (e.g. [112]). Hyperinsulinaemic hypoglycaemia can be treated through dietary modification and avoidance of foods with a high glycaemic index. Pharmacological therapies include acarbose, somatostatin analogues and diazoxide. The last resort, in the rare unresponsive cases, involves reduction in beta-cell mass through a partial pancreatectomy.

The RYGB, AGB and VSG procedures cause reductions in peripheral insulin resistance directly as a result of gradual weight loss [81]. However, in some human studies, hepatic insulin resistance is reduced within days after RYGB before any clinically significant weight loss has taken place (e.g. [25, 113]). Whilst this may be a direct result of a reduction in caloric intake [114], the reduction in hepatic insulin resistance in some studies is greater in patients after RYGB compared to patients undergoing similar caloric restriction after AGB or a hypocaloric diet [25, 84, 113

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