Obese subjects tend to consume a more energy-dense diet than normal-weight subjects.  Lancet. 1975 Nov 8;2(7941):905-6. The higher energy density results in more rapid gastric emptying of high energy food into the duodenum   Scand J Gastroenterol. 1993 Aug;28(8):737-43  as the compensatory response of gastric slowing in response to high density food is unfortunately incomplete in man. High energy foods with high energy drinks (burgers and coke) could thus result in a "relatively" rapid gastric emptying such that higher energy consumption occurs on this kind of a diet. Fat rich liquid meals tend to result in greater gastric emptying which has been correlated positively with the weight of subjects, although similar correlations were not noted for predominantly protein or carbohydrate based meals.

Intestinal motility (intestinal transit time), intestinal absorptive surface and enterocyte transport mechanisms can influence the digestion and absorption of energy from a meal. Intestinal motility is regulated by the activity of the migrating motor complex (MMC). MMC is a recurrent pattern of cyclically occurring motor activity which has three phases. Phase 1 activity in the intestine is characterised by motor quiescent activity. Phase II activity consists of irregular motor activity. Phase III is composed of short bursts of rhythmic contractions. Obese patients have a lower phase I activity with increased phase II activity,  Scand J Gastroenterol. 1992 Jul;27(7):538-44.  a state of increased contractility which is prominent in the fasted state in anticipation of the next meal, which could result in increased absorption of energy through a greater pre-absorptive processing of food. Phase III activity correlates well with motilin levels which has been reported to be lower in obese humans.  Fat seems to be a major regulatory factor of intestinal motility, increasing transit times as demonstrated by lipid infusions into the ileum.   Gastroenterology. 1984 Feb;86(2):274-80. Yet, intestinal motility may not be closely related to satiety as shown by satiety induction by lipid infusions into jejunum without alteration of intestinal motility.  Gut. 1988 Mar;29(3):306-11. Release of regulatory peptides which produce satiety by other mechanisms may account for this discrepancy. (see below)

Intestinal absorption of energy has been noted to be  greater in the obese Metabolism. 1992 Apr;41(4):390-5.  despite similar gastric emptying times and volumes. The autonomic system through the vagus may contribute in some unknown way to intestinal absorption. Vagotomy prevents development of obesity in the rats,  J Comp Physiol Psychol. 1977 Dec;91(6):1284-96.  and produces weight loss in morbidly obese humans through reduced food intake J Auton Nerv Syst. 1983 Oct;9(1):273-81.  which seems to be  independent of alteration of gastric emptying as demonstrated in rats.  Am J Physiol. 1979 Jan;236(1):R61-6.

Regulatory peptides released from the intestine might contribute to satiety induction.  Cholecystokinin (CCK ) which has an important role in satiety induction in the obese  Physiol Behav. 1982 Oct;29(4):627-30. and normal weight subjects  Am J Clin Nutr. 1981 Feb;34(2):154-60.   seems to be less effective in the obese with regard to gall bladder contractility and pancreatic enzyme secretion. Despite normal secretion of CCK in the obese in the fasted and postprandial state,  Regul Pept. 1992 Apr 29;39(1):43-54.   a relative insensitivity to its satiety inducing effects could contribute to increased energy intake in the obese.  Somatostatin which inhibits gastric emptying and intestinal motility    Digestion. 1981;22(3):126-37. could be a hormone that could be potentially be implicated in satiety induction via actions mediated through the vagus.   Obese patients tend to have a lower somatostatin release after meals,   Regul Pept. 1992 Apr 29;39(1):43-54.    but may well  have increased sensitivity to somatostatin.  J Intern Med. 1995 Apr;237(4):411-8.   Its physiological role in the pathogenesis or perpetuation of obesity is far from well characterised. Neurotensin secreted from the ileum predominantly in response to fat, normally decreases gastric emptying rate. But post-prandial Neurotensin levels are low in the obese, probably as a secondary effect rather than a primary factor involved in altering intestinal transit. Its effects on adipose tissue Ann N Y Acad Sci. 1982;400:183-97.   might have implications on fat storage,    while the effects on satiety demonstrated on central administration  Int Rev Neurobiol. 1985;27:207-98.    might contribute to feeding behaviour modification.  

It is still not clear whether changes of gastric and intestinal motility are primary or secondary changes in obesity. Weight loss does not seem to alter the gastric emptying rate  Gastroenterology. 1983 Apr;84(4):747-51.  and hence it is possible that alterations in gastrointestinal motility could be a primary event facilitating weight gain.  Presently available data though enlightening are yet confusing due to contradictory results, produced probably secondary to uncontrolled and unrecognised confounding factors. While gastric emptying can account for up to 35% of the variability in postprandial glucose levels, the existing glycaemia can in turn influence gastric emptying. Hyperglycaemia(>15 mmol/L) has been known to delay gastric emptying in type I patients  Diabetologia. 1990 Nov;33(11):675-80.   with a similar reduction in motility noted in type 2 patients as well.  Diabetologia. 1989 Mar;32(3):151-9. On the other hand, hypoglycaemia accelerates gastric emptying probably as a counter regulatory response. Diabet Med. 1993 Aug-Sep;10(7):660-3.  Confounding factors as these will  have to be identified and adjusted for in interpreting gastric motility assessments in the obese.

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