Many thousands of years ago, our ancestors were hunter– gatherers and performed arduous labor. They hunted animals and also ate some fibrous roots, berries, and nuts—a diet high in protein with some complex carbohydrates [1–3]. This coincides with a diet with a low glycemic index [4, 5]. These meals were irregular and sometimes infrequent, and when there was a “kill”, the entire clan would share the meal. Through natural selection, early man developed “thrifty” genes for times of famine [6]. However, in the past 8,000 years, farming of indigenous wild grains commenced. Frequent high carbohydrate meals with a higher glycemic index became available, with frequent stimulation of insulin secretion from the pancreas. High plasma insulin levels and insulin resistance developed, with impaired glucose tolerance. This progressed to the modern era where fast foods (containing particularly high levels of simple sugars), affluence, and a sedentary lifestyle have led to an “obesity pandemic”. The so-called metabolic syndrome, with insulin resistance, type 2 diabetes, hypertension, dyslipidemia, atherosclerosis, and coronary artery disease, and fatty liver are now prevalent [7]. The prior thrifty genes now contribute to obesity. We now have the increasing incidence of type 2 diabetes. The impaired glucose handling is associated with elevated plasma insulin and a down-regulation of insulin receptors [8]. The high levels of circulating insulin inhibit lipolysis and promote lipogenesis. Immediately following all types of bariatric operations, there is rapid improvement in glucose handling, before there is significant weight loss and often before the patient is even discharged from hospital [9, 10]. After the old jejuno-ileal bypass, the oral glucose tolerance and insulin tolerance curves were markedly flattened—glucose bypassed its absorptive area in the intestine [11]. Shortly after gastric restrictive or gastric bypass operations with gastric channel and stomal edema, the patient is only able to consume 575±146 kcal/day at time of discharge from hospital [12–14] and there is rapid up-regulation of insulin receptors [15, 16] located on cell membranes in muscle and adipose tissue. Later, the improved glucose metabolism after gastric restrictive [17] and bypass [18] procedures is associated with the weight loss, and is greater after gastric bypass operations, which are followed by a more rapid and greater decrease in fat mass [9]. Originally, bypass of hormones in the foregut was postulated as the reason for the improved glucose processing [19, 20]. More recently, stimulation of incretins (intestinal hormones that stimulate insulin secretion) in the distal small bowel due to expedited nutrient delivery, have been confirmed to be elevated [21]. The most interest has been in glucagon-like peptide-1 (GLP-1) secreted into the bloodstream by the L-cells of the hindgut [22, 23]. GLP-1 (7-36) amide has been found to stimulate postprandial OBES SURG (2008) 18:1211–1214 DOI 10.1007/s11695-008-9674-9
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Sep 1, 2023
Devajit Mohajan + 1
Open Access
