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Two hundred twenty dietitians participated in a workshop conference on Health Implications of Dietary Fiber. They were given lectures to increase their knowledge base, and then in group sessions answered questions and wrote concensus opinions. The results are the content of this paper. The topics covered and responses are reported in four categories, diabetes and obesity, hyperlipidemia, hypertension and coronary heart disease, gut function and gastrointestinal disease, and cancer. Specific recommendation for implementing high fiber diets are made in each category. However, the dietitians expressed caution on accepting all of the conclusions expressed in the literature on the value of fiber and believed much education and instruction is needed in order to increase dietary fiber intake.
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PMID:Practical aspects of implementing increased dietary fiber intake. 302 Sep 72

Surgical manipulations of the gastrointestinal system can have a major impact on the ingestive behavior of animals. Particularly well-documented are the feeding and drinking effects of JIB and vagotomy. These two surgical procedures are similar in that they reduce the food intake and body weight of obese animals more than that of lean animals, and of hypothalamic obese rats more than that of genetically obese rats. Intermediate effects are obtained with other obesity models. Given the multiple etiologies of human obesity, it is not surprising that gastrointestinal surgery has variable effects in obese humans. The effects of gastric surgery on the ingestive behavior of animals have received relatively little attention. This is unfortunate because gastric bypass is now one of the most widely used methods for surgical treatment of human obesity. In light of recent developments in gastric surgical techniques and new findings concerning the gastric modulation of food intake, the effects of gastric surgery on the feeding behavior of animals should be further investigated. Much remains to be learned about the physiologic and behavioral mechanisms by which gastrointestinal surgery influences ingestive behavior and body weight. Surgical manipulations of the gastrointestinal system may affect ingestive behavior by directly altering the neural and hormonal feedback signals to the brain from the stomach, intestines, and other organs (liver, pancreas), or they may indirectly alter these feedback signals by modifying the preabsorptive and/or postabsorptive flow of nutrients. Seen from a functional perspective, the gut sends to the brain different types of messages that modulate ingestive behavior. Most attention has focused on gut satiety signals, but the gut can also be the source of painful sensations that suppress ingestive behavior. The distinction between satiety and discomfort is not always clear-cut. For example, gut distention may be satiating when it is moderate, but painful when it is extreme. Nevertheless, the distinction is an important one, and the nature of the feeding-inhibitory effects obtained in animal studies must be carefully evaluated. Ideally, obesity surgery should produce minimal aversive consequences, although whether it is possible to reduce food intake and body weight without producing any discomfort remains to be established. In addition to being a source of feeding-inhibitory cues, the gastrointestinal system may also provide excitatory cues that stimulate feeding and modify food preferences. For example, intestinal infusions of carbohydrates increase subsequent food intake under certain conditions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of gastrointestinal surgery on ingestive behavior in animals. 332 27

The occurrence of cholesterol malabsorption and its role in the regulation of cholesterol metabolism were studied in 30 patients with an earlier gut resection and 9 patients with a jejunoileal bypass for treatment of obesity. Fractional cholesterol absorption varied from 0.1% to 70%, and was lowest in jejunoileal bypass (8.3%) associated with severe fat and moderate bile acid malabsorptions and in 15 patients with a long small-intestinal resection (20.4%) associated with severe bile acid and moderate fat malabsorption. Seven resected patients with normal fecal fat and bile acids and 8 resected patients with malabsorption of only bile acid had normal cholesterol absorption. Low fractional cholesterol absorption was associated with a short length of the remaining proximal small intestine, high dietary intake of plant sterol, and high fecal fat and neutral sterol excretions, but not with bile acid malabsorption. In the whole study population, plasma levels of total, low-density lipoprotein, and high-density lipoprotein cholesterol were positively correlated with fractional cholesterol absorption and the amount of total, dietary, and biliary absorbed cholesterol and were negatively correlated with fecal cholesterol elimination as neutral sterols (less so as bile acids) and cholesterol synthesis. The results emphasize that, in patients with ileal exclusion, plasma levels of low-density lipoprotein and high-density lipoprotein cholesterol are regulated more effectively by cholesterol than by bile acid malabsorption. Moreover, although the fecal loss of bile acids is the main determinant in cholesterol elimination and stimulation of cholesterol synthesis in patients with intestinal exclusions, intestinal cholesterol absorption also contributes noticeably to the regulation of cholesterol synthesis.
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PMID:Cholesterol absorption regulates cholesterol metabolism and plasma lipoprotein levels in patients with gut exclusions. 333 31

Food can affect the production and secretion of hormones by direct actions on the gut, by nervous reflexes, through changes in the concentration of various metabolites in the blood, or secondary to changes in circulating gut hormone levels. Not only is the composition of the diet important but also its texture, quantity and duration. GIP and insulin are used as examples of hormones whose production and secretion are diet-dependent. Their possible involvement in the pathogenesis of obesity and non-insulin-dependent (type II) diabetes is discussed.
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PMID:How our food affects our hormones. 388 42

The effects of portacaval anastomosis (PCA) on cholesterol biodynamics of male adult (fa/fa) Zucker rats and their lean littermates were studied with an isotopic equilibrium method. Animals were fed with a sucrose-rich semi-purified diet. Obese rats were hypercholesterolemic (2.03 +/- 0.14 vs 1.06 +/- 0.7 mg/ml), had a cholesterol-enriched liver (135.3 +/- 14.5 vs 40.0 +/- 2.6 mg/liver) and accumulated cholesterol in body pools. However no difference in the rates of cholesterol absorption, synthesis, fecal elimination or transformation into bile acids distinguished obese from lean Zucker rats. In both lean and obese rats, PCA decreased cholesterolemia by about 28 per cent and liver weight by 40 per cent while the total cholesterol content of the liver was not affected. Input of synthesized cholesterol (internal secretion) was strikingly decreased by the shunt (from 13.2 +/- 0.6 and 12.6 +/- 0.7 mg/day/rat before PCA, to 8.9 +/- 0.8 and 8.6 +/- 1.0 mg/day/rat after PCA) in lean and obese rats respectively. A similar decrease was observed in the cholesterol transformation into bile acids. Since the activity of the gut for cholesterol synthesis, as shown by the fecal external secretion (cholesterol synthesized by the gut and directly eliminated in the gut and feces) was probably not modified, the reduction of internal secretion induced by PCA resulted from decreased hepatic cholesterogenesis. It is suggested that this decrease may be one of the factors involved in the lowering effect of PCA on plasma cholesterol level.
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PMID:Cholesterol metabolism in lean and obese Zucker rats: effects of portacaval anastomosis. 401 13

The available data show that GIP is at present the strongest candidate for the insulin-secreting factor of the gut named incretin. Its release is triggered by the absorption of ingested nutrients. GIP acts on the B-cells of the pancreas by potentiating glucose-induced insulin secretion. The role of GIP as an enterogastrone is less well established. The release of GIP from the gut cells seems to be regulated by the composition and the amount of the ingested food, by the rate of absorption of nutrients by neural factors (vagal), and by feedback control mediated by insulin. In addition, the adaptation of the intestine to individual eating habits influences the response of the GIP cells. It is suggested that an overactive enteroinsular axis, i.e. enhanced GIP secretion, participates in the development of the hyperinsulinaemia of obesity and maturity onset diabetes mellitus. In gastrointestinal diseases accompanied by malabsorption the GIP response is diminished. In gastrointestinal disorders with rapid gastric emptying (duodenal ulcer) or with accelerated passage of the nutrients through the intestine, hypersecretion of GIP and insulin occurs. This may be significant for the reactive hypoglycaemia of these conditions.
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PMID:Gastric inhibitory polypeptide. 610 91

Normal, male Sprague-Dawley (S-D) rats and female, lean and obese Zucker rats were studied in the fed state and after 48 hours of food deprivation. Somatostatin-like immunoreactivity (SLI) was measured from acetic acid extracts of oesophagus-cardia, stomach, small and large intestine, pancreas, hypothalamus, pituitary and cerebellum. Within the CNS, the highest levels of SLI were found in the hypothalamus, while in the gut, these levels were highest in the stomach and pancreas. All Zucker rats displayed higher hypothalamic levels of SLI than did S-D rats. Obese Zucker rats in the fed state differed from their lean littermates in that SLI levels were lower in oesophagus-cardia, stomach and hypothalamus, while being higher in pancreas and pituitary. The response to starvation in both obese and lean Zucker rats was qualitatively similar, and included significant increases in stomach and oesophagus-cardia SLI, but with a significant fall hypothalamic SLI. We have concluded that the increase in gastrointestinal SLI with starvation in Zucker as well as in S-D rats may represent a significant regulatory mechanism in nutrient homeostasis. We postulate that gastric SLI may decrease the availability of intestinal insulin secretagogues in the fasting state. This adaptive mechanism appears to be intact in the obese Zucker rat.
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PMID:Starvation increases gastrointestinal somatostatin in normal and obese Zucker rats: a possible regulatory mechanism. 612 4

In the past 10 years, numerous gut peptides have been tested for their satiating effect on food intake. Cholecystokinin (CCK), bombesin, pancreatic glucagon, and somatostatin have the best supporting evidence for such a specific behavioral effect. The satiety effect of CCK, somatostatin, and glucagon is abolished or markedly reduced by abdominal vagotomy, but the satiety effect of bombesin is not. The effect of vagotomy has been interpreted as the result of the loss of vagal afferent fibers that are necessary for carrying information about visceral effects of these peptides to the brain. This hypothesis is under active investigation. There are three reports that CCK decreases the size of a test meal in lean and obese humans. This suggests that CCK or the other peptides may be useful in treating human obesity and bulimia.
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PMID:Gut peptides and postprandial satiety. 614 53

Cholecystokinin (CCK) acts acutely to inhibit food consumption in fasted rats, mice, sheep, pigs, monkeys and humans. CCK has been proposed as a satiety signal, inducing the behavioural sequence of satiety, or as an aversive internal stimulus, which inhibits food intake by inducing malaise. Reductions in food intake and related exploratory behaviours are initiated by CCK at its peripheral receptor in the gut, which appears to transmit sensory feedback via the vagus nerve to brain regions mediating appetitive behaviours. The therapeutic potential of CCK as an appetite suppressant in obesity syndromes rests on the demonstration of significant, long-lasting body weight reduction. Chronic CCK administration by repeated injections is problematic, since this peptide is rapidly degraded in vivo. We chose the Alzet constant infusion osmotic minipump to investigate possible alterations in body weight and food intake during continuous infusion of CCK. We now report that no change was detected in either body weight or total daily food consumption at any time point during 2 weeks of intraperitoneally (i.p.) infused CCK. The mechanism underlying the lack of chronic CCK effects appears to be a rapid development of behavioural tolerance. Acute challenge doses of CCK which induced satiety-related behaviours in saline-infused rats were ineffective in CCK-infused rats. The behavioural tolerance was apparent within a few hours of minipump implantation. These results provide the first evidence that rapid and reversible tolerance develops to the actions of a gut peptide.
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PMID:Rapid development of tolerance to the behavioural actions of cholecystokinin. 630 Jun 93

The entero-insular axis comprises direct substrate stimulation of the islet cells by the absorbed nutrients and signal transmission by endocrine factors and nerves. The extent of neural influences has not yet been evaluated. GIP is the main incretin candidate. GIP release is dependent on nutrient absorption. Therefore, GIP abnormalities occur in a large number of gastrointestinal and metabolic diseases. These secondary changes are rarely of clinical significance. GIP hypersecretion may, however, contribute to the increased lipogenesis in obesity and the hypoglycemia in the late dumping syndrome. In type II diabetes hyper- and hyposecretion of GIP has been found but no correlation between GIP and insulin response. GIP abnormalities are not identical with disturbances of the entero-insular axis. These can only be evaluated by estimating the incretin effect (comparing the insulin response to oral glucose with the insulin response to an isoglycaemic iv glucose infusion). A decreased incretin effect has been observed in patients with jejuno-ileal bypass and in type II diabetes. In neither condition was a correlation found between incretin effect and GIP response. It is concluded that disturbances of the entero-insular axis are rarely explained by GIP abnormalities. Therefore, other humoral gut factors must exist. Also the neural part of the entero-insular axis requires exploration in health and disease.
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PMID:Disturbances of the entero-insular axis. 635 14


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