Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dietary modification is useful in both type 1 and type 2 diabetes. Glucose levels after a meal are largely determined by carbohydrate intake. Decreased intake of simple carbohydrates and increased fiber consumption lower postprandial glucose. Obesity has become epidemic in the United States and has dramatically increased the incidence of type 2 diabetes by augmenting insulin resistance. Dietary treatment of obesity has been frustrating. Success will require education in using foods with high fiber contents, low glycemic indexes, and low saturated fat levels. The use of natural foods must be supplemented by the use of semisynthetic foods with desirable properties. The educational efforts required are substantial and must be recognized by third-party reimbursement agencies. Operative procedures to decrease intake or reduce the absorption of food are being used with increasing frequency. Bariatric surgery is often successful in inducing a substantial loss of weight; however, this success must be balanced against the complications of surgery, which can be considerable. The pharmacologic approaches to treatment of obesity have focused primarily on anorexigenic agents. Several polypeptides that induce satiety are currently under study, including leptin and glucagon-like peptide-1 (GLP-1). Orlistat has been used to induce the malabsorption of fat to reduce caloric ingestion. Of the currently used oral hypoglycemics, metformin and the disaccharidase inhibitors have the best tendency to promote weight loss. There is active research on the uncoupling proteins that induce thermogenesis and promote the dissipation of calories. The beta-3 agonists act through the uncoupling proteins. The thiazolidinediones tend to promote weight gain through the PPAR gene locus. Agents that antagonize this effect could induce weight loss. The future will undoubtedly bring us drugs that are effective in causing weight loss. The advent of drugs to successfully combat obesity will substantially improve public health.
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PMID:Advances in diabetes for the millennium: nutritional therapy of type 2 diabetes. 1564 15

The proglucagon-derived peptide glucagon-like peptide-1 (GLP-1) is an intestinal signal peptide postprandially released from the L cells of the lower gut. Exogenously administered the synthetic hormone exerts a glucose-dependent insulinotropic effect at the pancreatic beta-cells and lowers plasma glucagon by an inhibitory effect against the alpha-cells. It delays gastric emptying by relaxation of the gastric fundus, inhibition of antral contractility, and stimulation of both the tonic and phasic motility of the pyloric sphincter. Enhancement of insulin, suppression of glucagon, and inhibition of gastric emptying are the main determinants controlling glucose homeostasis with GLP-1. Human studies employing the specific GLP-1 receptor antagonist exendin(9-39) show that endogenously released GLP-1 likewise controls fasting plasma glucagon, stimulates insulin, and influences all the motoric mechanisms known to control gastric emptying. Therefore, GLP-1 is discussed as an incretin hormone and as an enterogastrone in man. Synthetic GLP-1 also suppresses gastric acid and pancreatic enzyme secretion. The inhibitory effects on upper gastrointestinal functions are at least partly mediated by vagal-cholinergic inhibition and may involve interactions with vagal afferent pathways and/or circumventricular regions within the CNS. GLP-1 is a candidate humoral mediator of the 'ileal brake' exerting inhibition of upper gastrointestinal function preventing malabsorption and postprandial metabolic disturbances. As human studies indicate a central action of GLP-1 in reduction of food intake, it is uncertain if this is a consequence of induction of satiety or of transduction of visceral aversive stress signals.
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PMID:The physiological role of GLP-1 in human: incretin, ileal brake or more? 1578 Apr 30

Diarrhoea, malabsorption and malnutrition characterise the short bowel syndrome. The underlying gastrointestinal disorders, the types of intestinal resections performed and the subsequent pathophysiological situations are reviewed. Recommended therapeutic measures in the postoperative period as well as in the rehabilitation of patients with short bowel syndrome are discussed in more detail. In the postoperative period, parenteral nutrition is essential followed by an enteral diet to stimulate bowel adaptation, reduce fluid loss and increase nutrient absorption. The final diet should be based on the anatomy of the retained bowel (presence or absence of a colon and ileum). The importance of the colon as a digestive organ in patients with short bowel and the need of a low-oxalate diet are underlined. The possible benefit of new treatment options (glutamine, growth hormone and glucagon-like peptide 2) is discussed. Both typical complications of the short bowel syndrome and management of these complications are presented.
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PMID:[Clinical management of patients with short bowel syndrome]. 1600 49

Multiple peptide hormones produced within the gastrointestinal system aid in the regulation of energy homeostasis and metabolism. Among these is the intestinotrophic peptide glucagon-like peptide-2 (GLP-2), which is released following food intake and plays a significant role in the adaptive regulation of bowel mass and mucosal integrity. The discovery of GLP-2's potent growth-promoting and cytoprotective effects in the gastrointestinal (GI) tract stimulated interest in its use as a therapeutic agent for the treatment of GI diseases involving malabsorption, inflammation, and/or mucosal damage. Current research has focused on determining the physiological mechanisms contributing to the effects of GLP-2 and factors regulating its biological mechanisms of action. This chapter provides an overview of the biology of GLP-2 with a focus on the most recent findings on the role of this peptide hormone in the normal and diseased GI tract.
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PMID:Glucagon-like Peptide-2. 1660 31

Short bowel syndrome (SBS) is used to describe a condition of malabsorption and malnutrition resulting from the loss of absorptive area following massive small bowel resection. The key to improved clinical outcome after massive small bowel resection is the ability of the residual bowel to adapt. Although still in experimental stages, a major goal in the management of SBS may be the augmented use of growth factors to promote increased adaptation. A number of growth factors have been implicated in promoting the adaptation process. The best-described growth factors are reviewed: glucagon-like peptide-2 (GLP-2), epidermal growth factor (EGF), and growth hormone (GH). This article reviews the ability of recombinant GLP-2, EGF and GH to modulate structural and functional aspects of intestinal adaptation following small bowel resection. Although these growth factors have shown promise, small sample size, inconsistent measurement parameters and uncontrolled study designs have hampered the acquisition of strong data advocating the use of growth factor treatment for SBS. Multicenter trials using well-defined outcome measures to assess clinical efficacy are needed to direct the clinical indications, timing and duration of therapy and assess potential risks associated with growth factor therapies.
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PMID:New growth factor therapies aimed at improving intestinal adaptation in short bowel syndrome. 1672 75

Despite dramatically increased research efforts to discover cures for the rising health issue of obesity, bariatric (obesity) surgery remains the most effective treatment. Obese people and especially those classified as morbidly obese often suffer from associated co-morbid conditions such as type-II diabetes. In most cases, bariatric surgery results in rapid and sustained decreases in excess body weight. Recent reports have identified significant improvements in glucose homeostasis after surgery that are coincident and often precedent to any measurable weight loss. These studies suggest an inhibition or enhancement of a "factor" within the intestinal tract that improves glycemia independent of body fat stores. These observations have sparked renewed investigation into the mechanisms underlying successful obesity surgeries such as gastric bypass. It is becoming increasingly clear that restriction and malabsorption are not the only two mechanisms important for inducing long-term weight loss or the improvements in diabetes. Investigating the hypothesis that the distal intestine (ileum) holds additional answers into a third mechanism, I used the model of ileal transposition to help identify endocrine changes in the gut following obesity surgery. This review will explore the model of ileal transposition and speculate on its usefulness as a tool to dissect out additional mechanisms underlying effective obesity surgeries. Also discussed will be the ileal-produced hormone glucagon-like peptide and its role in mediating the improvements in diabetes and weight loss after bariatric surgery.
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PMID:Ileal transposition provides insight into the effectiveness of gastric bypass surgery. 1678 38

Short bowel syndrome (SBS) refers to the malabsorption of nutrients, water, and essential vitamins as a result of disease or surgical removal of parts of the small intestine. The most common reasons for removing part of the small intestine are due to surgical intervention for the treatment of either Crohn's disease or necrotizing enterocolitis. Intestinal adaptation following resection may take weeks to months to be achieved, thus nutritional support requires a variety of therapeutic measures, which include parenteral nutrition. Improper nutrition management can leave the SBS patient malnourished and/or dehydrated, which can be life threatening. The development of therapeutic strategies that reduce both the complications and medical costs associated with SBS/long-term parenteral nutrition while enhancing the intestinal adaptive response would be valuable. Currently, therapeutic options available for the treatment of SBS are limited. There are many potential stimulators of intestinal adaptation including peptide hormones, growth factors, and neuronally-derived components. Glucagon-like peptide-2 (GLP-2) is one potential treatment for gastrointestinal disorders associated with insufficient mucosal function. A significant body of evidence demonstrates that GLP-2 is a trophic hormone that plays an important role in controlling intestinal adaptation. Recent data from clinical trials demonstrate that GLP-2 is safe, well-tolerated, and promotes intestinal growth in SBS patients. However, the mechanism of action and the localization of the glucagon-like peptide-2 receptor (GLP-2R) remains an enigma. This review summarizes the role of a number of mucosal-derived factors that might be involved with intestinal adaptation processes; however, this discussion primarily examines the physiology, mechanism of action, and utility of GLP-2 in the regulation of intestinal mucosal growth.
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PMID:Gut hormones, and short bowel syndrome: the enigmatic role of glucagon-like peptide-2 in the regulation of intestinal adaptation. 1683 Mar 59

Necrolytic migratory erythema (NME) is an uncommon inflammatory dermatosis with a distinctive clinical and histological appearance. It shows irregular erythema, bullae, erosion, crusts and pigmentation. While it is typically associated with glucagonoma, some cases of NME without glucagonoma have been reported. Herein, we report a case of necrolytic migratory erythema associated with malabsorption 30 years after ileocolectomy. She presented erosive erythema with scale or partly flaccid bullae on her intergluteal cleft, buttock and extremities. Her laboratory data revealed essential amino acid deficiency and a slightly decreased serum zinc level, while her plasma glucagon level was low. With diagnosis of non-glucagonoma-associated NME with malabsorption due to short-bowel syndrome, she was treated and improved by i.v. amino acid supplement. Histological findings of NME include necrotic changes of keratinocytes in the upper epidermis, proliferation of those in the lower epidermis and inflammatory cell infiltration of upper dermis. We also examined the expression pattern of epidermal keratins (K6, K10) and Ki-67, one of the markers of proliferative activity, to assess the proliferation and differentiation of keratinocytes in a NME lesion by immunostaining. The findings with these immunostainings support the characteristics of HE-staining, and suggest hyponutrition may induce changing differentiation/proliferation of keratinocytes.
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PMID:Necrolytic migratory erythema without glucagonoma in a patient with short bowel syndrome. 1692 38

Type 1 diabetes is an intrinsically unstable condition. However, the term "brittle diabetes" is reserved for those cases in which the instability, whatever its cause, results in disruption of life and often recurrent and/or prolonged hospitalization. It affects 3/1000 insulin-dependent diabetic patients, mainly young women. Its prognosis is poor with lower quality of life scores, more microvascular and pregnancy complications and shortened life expectancy. Three forms have been described: recurrent diabetic ketoacidosis, predominant hypoglycemic forms and mixed instability. Main causes of brittleness include malabsorption, certain drugs (alcohol, antipsychotics), defective insulin absorption or degradation, defect of hyperglycemic hormones especially glucocorticoid and glucagon, and above all delayed gastric emptying as a result of autonomic neuropathy. Psychosocial factors are very important and factitious brittleness may lead to a self-perpetuating condition. The assessment of brittle diabetes requires quantification of the variability of blood glucose levels. To quantify instability, measures which have been developed, include Mean Amplitude of the largest Glycemic Excursions (MAGE), Mean Of Daily Differences (MODD), Lability Index (LI), Low Blood Glucose Index (LBGI), Clarke's score, Hyposcore, and continuous blood glucose monitoring. Once psychogenic problems have been excluded, therapeutic strategies require firstly, the treatment of underlying organic causes of the brittleness whenever possible and secondly optimising standard insulin therapy using analogues, multiple injections and consideration of Continuous Subcutaneous Insulin Infusion. Alternative approaches may still be needed for the most severely affected patients. Isolated islet transplantation (IIT), which restores glucose sensing, should be considered in cases of hypoglycaemic unawareness and/or lability especially if the body mass index is < 25, but with current immunosuppressive protocols patients must have normal renal function and preferably no plans for pregnancy. Implantable pumps have advantages for patients who either weigh more than 80 kgs or have abnormalities of kidney or liver function or are highly sensitised.
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PMID:Management strategies for brittle diabetes. 1707 32

Over the lifetime of the animal, there are many changes in the function of the body's organ systems. In the gastrointestinal tract there is a general modest decline in the function of the esophagus, stomach, colon, pancreas and liver. In the small intestine, there may be subtle alterations in the intestinal morphology, as well as a decline in the uptake of fatty acids and sugars. The malabsorption may be partially reversed by aging glucagon-like peptide 2 (GLP2) or dexamethasone. Modifications in the type of lipids in the diet will influence the intestinal absorption of nutrients: for example, in mature rats a diet enriched with saturated as compared with polysaturated fatty acids will enhance lipid and sugar uptake, whereas in older animals the opposite effect is observed. Thus, the results of studies of the intestinal adaptation performed in mature rats does not necessarily apply in older animals. The age-associated malabsorption of nutrients that occurs with aging may be one of the several factors which contribute to the malnutrition that occurs with aging.
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PMID:Aging and the intestine. 1717 84


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