Traditionally, the weight loss achieved by bariatric surgery has been attributed to either a restriction of food intake or malabsorption of unrestricted oral consumption. This simplistic approach, of course, ignores the minimal weight loss success achieved by electronic stimulation procedures [2, 3, 16] that employ no overt restriction of eating or of absorption. In the final analysis, at the level of caloric absorption from the intestinal tract, all the common bariatric surgery procedures are restrictive. This principle is illustrated in Fig. 8.1a of the steps in ostensibly restrictive bariatric surgery and in Fig. 8.1b of the steps in ostensibly malabsorptive bariatric surgery. Caloric intake can be restricted by the inhibition of eating caused by a gastric balloon, a gastric band, a sleeve gastrectomy, or a gastric bypass. Caloric intake can be equally restricted by the insufficient intestinal absorptive surface available in the so-called malabsorptive procedures. Since the bariatric surgery operations, even those with the ultrashort common channels of a biliopancreatic diversion or duodenal switch, extremely rarely cause excessive weight loss, there must be a brake effect in body metabolism not explainable by the old mechanisms of action concepts. Further, there are many nonobese, even lean, individuals who have undergone gastric or massive intestinal resections for various reasons and who subsequently maintained their body weight. It is time, therefore, in order to understand the changes we are eliciting by metabolic bariatric surgery, that we acknowledge that we do restrict the ability to eat and that we do restrict body caloric intake, but that we must look to more sophisticated explanations for the true mechanisms of action of these procedures. We need to investigate the complex neurohormonal networks that control weight, certain weight-related diseases, and the disease of obesity itself.

Having defined metabolic surgery, we should now more closely examine the energy metabolism of obesity, the primary working domain of metabolic/bariatric surgery. Past knowledge of obesity causation and mechanisms of action focused on genetics and energy balance [94, 95]. The genetics of obesity is not truly a subject to be covered under metabolic surgery or metabolics; however, energy balance is appropriately considered under metabolic mechanisms.

Total body metabolic processes in kinetic terms can be defined as total energy expenditure (TEE), which is equal to the basal metabolic rate (BMR), the energy of activity expenditure, the thermal effect of food (TEF), and adaptive thermogenesis (AT). The BMR is the lowest level of energy needed to maintain life (e.g., autonomic cardiorespiratory functions). The TEF is the body heat produced and the AT is the fluctuation in TEF produced by environmental temperature and humidity [95]. The homeostatic responses to increased food intake in normal individuals essentially is an attempt to resist weight gain; whereas, in obese individuals these mechanisms appear to be blunted resulting in a decrease in the TEF and a subsequent decrease in the TEE [96].

The nature of energy metabolism after metabolic/bariatric surgery has not been extensively studied and is not well understood. The preoperative TEE of patients undergoing gastric bypass can vary from normal to hypermetabolic. In the former, there appears to be no change postoperatively; in the latter, normalization of TEE seems to occur postoperatively [97]. Further, preservation of energy economy is reciprocal to the degree of weight loss [98]. After gastric bypass, both TEE and resting energy expenditure are decreased by about 25 % [99].

Currently, underlying causative mechanisms for obesity and type 2 diabetes are often focused on the state of inflammation. An increase in energy (caloric) intake over energy expenditure leads to an increase in the size of the adipocytes. Once the adipocyte volume exceeds 1 μl of lipid, the number of fat cells increases. The ensuing leptin response in non-obese individuals reduces hunger and downregulates caloric intake. In the obese, with a blunted leptin response [71], the unchecked caloric load overtaxes the adipocytes’ ability to grow larger or increase in number resulting in a state of inflammation at the cellular level and ectopic fat storage in internal organs, including the liver and muscle [76]. In addition, the consumption of high volumes of fructose, absent in our ancestral diets, has been suggested to cause leptin resistance and elevated triglycerides, which result in weight gain [72, 100, 101] and a state of generalized inflammation.

The inflammation rationale carries over to obesity-induced type 2 diabetes. The increased fat cell mass results in an increase in free fatty acids, which, in turn, reduce glucose utilization by the liver and peripheral tissues, thereby reducing insulin clearance by the liver and increasing insulin delivery to the periphery, resulting in peripheral insulin resistance. Adipocyte-secreted cytokines contribute to the inflammatory state as well. The reactive oxygen species engendered by the inflammatory process are then responsible for endothelial damage, impaired beta cell function and, in general, play a cardinal role in the long-term complications of type 2 diabetes [102].