Database : MEDLINE
Search on : fructose and intolerance [Words]
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[PMID]: 29181545
[Au] Autor:Schnedl WJ; Lackner S; Enko D; Schenk M; Mangge H; Holasek SJ
[Ad] Address:Institute of Pathophysiology, Centre for Molecular Medicine, Medical University of Graz, Heinrichstrasse 31a, 8010, Graz, Austria. w.schnedl@dr-schnedl.at.
[Ti] Title:Non-celiac gluten sensitivity: people without celiac disease avoiding gluten-is it due to histamine intolerance?
[So] Source:Inflamm Res;67(4):279-284, 2018 Apr.
[Is] ISSN:1420-908X
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Food intolerance/malabsorption is caused by food ingredients, carbohydrates (mainly lactose and fructose), proteins (gluten), and biogenic amines (histamine) which cause nonspecific gastrointestinal and extra-intestinal symptoms. Here we focus on possible etiologic factors of intolerance/malabsorption especially in people with non-celiac gluten sensitivity (NCGS) or the so-called people without celiac disease avoiding gluten (PWCDAG) and histamine intolerance. METHODS: Recognizing the recently described symptoms of NCGS (PWCDAG) we review correlations and parallels to histamine intolerance (HIT). RESULTS: We show that intestinal and extra-intestinal NCGS (PWCDAG) symptoms are very similar to those which can be found in histamine intolerance. CONCLUSIONS: After a detailed diagnostic workup for all possible etiologic factors in every patient, a targeted dietary intervention for single or possibly combined intolerance/malabsorption might be more effective than a short-term diet low in fermentable oligo-, di- and monosaccharides and polyols (FODMAP) or the untargeted uncritical use of gluten-free diets.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1711
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process
[do] DOI:10.1007/s00011-017-1117-4

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[PMID]: 29510902
[Au] Autor:Li H; Byers HM; Diaz-Kuan A; Vos MB; Hall PL; Tortorelli S; Singh R; Wallenstein MB; Allain M; Dimmock DP; Farrell RM; McCandless S; Gambello MJ
[Ad] Address:Department of Human Genetics, School of Medicine, Emory University, Atlanta, GA, United States; Department of Pediatrics, School of Medicine, Emory University, Children's Healthcare of Atlanta, Atlanta, GA, United States. Electronic address: Hong.Li@emory.edu.
[Ti] Title:Acute liver failure in neonates with undiagnosed hereditary fructose intolerance due to exposure from widely available infant formulas.
[So] Source:Mol Genet Metab;, 2018 Feb 27.
[Is] ISSN:1096-7206
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Hereditary fructose intolerance (HFI) is an autosomal recessive disorder caused by aldolase B (ADOLB) deficiency resulting in an inability to metabolize fructose. The toxic accumulation of intermediate fructose-1-phosphate causes multiple metabolic disturbances, including postprandial hypoglycemia, lactic acidosis, electrolyte disturbance, and liver/kidney dysfunction. The clinical presentation varies depending on the age of exposure and the load of fructose. Some common infant formulas contain fructose in various forms, such as sucrose, a disaccharide of fructose and glucose. Exposure to formula containing fructogenic compounds is an important, but often overlooked trigger for severe metabolic disturbances in HFI. Here we report four neonates with undiagnosed HFI, all caused by the common, homozygous mutation c.448G>C (p.A150P) in ADOLB, who developed life-threatening acute liver failure due to fructose-containing formulas. These cases underscore the importance of dietary history and consideration of HFI in cases of neonatal or infantile acute liver failure for prompt diagnosis and treatment of HFI.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:Publisher

  3 / 868 MEDLINE  
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[PMID]: 29502917
[Au] Autor:Demirbas D; Brucker WJ; Berry GT
[Ad] Address:Division of Genetics and Genomics, Boston Children's Hospital, Harvard Medical School, Center for Life Science Building, 3 Blackfan Circle, Boston, MA 02115, USA.
[Ti] Title:Inborn Errors of Metabolism with Hepatopathy: Metabolism Defects of Galactose, Fructose, and Tyrosine.
[So] Source:Pediatr Clin North Am;65(2):337-352, 2018 Apr.
[Is] ISSN:1557-8240
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The liver is one of the most essential organs in metabolism and is responsible for metabolizing a wide variety of molecules from amino acids to sugars. Although it is responsible for many essential metabolic processes, it is one of the most severely affected by metabolic disease because, in many cases, it is the first to be exposed to the toxic intermediates. The metabolism of galactose, fructose, and tyrosine involve the liver and although there are systemic findings in metabolic disease involved with these substrates, severe hepatopathy is a common presenting aspect of galactosemia, hereditary fructose intolerance, and tyrosinemia type I.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[St] Status:In-Data-Review

  4 / 868 MEDLINE  
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[PMID]: 29502266
[Au] Autor:Janssen AWF; Katiraei S; Bartosinska B; Eberhard D; Willems van Dijk K; Kersten S
[Ad] Address:Nutrition, Metabolism and Genomics Group, Division of Human Nutrition and Health, Wageningen University, Stippeneng 4, 6708 WE, Wageningen, the Netherlands.
[Ti] Title:Loss of angiopoietin-like 4 (ANGPTL4) in mice with diet-induced obesity uncouples visceral obesity from glucose intolerance partly via the gut microbiota.
[So] Source:Diabetologia;, 2018 Mar 03.
[Is] ISSN:1432-0428
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:AIMS/HYPOTHESIS: Angiopoietin-like 4 (ANGPTL4) is an important regulator of triacylglycerol metabolism, carrying out this role by inhibiting the enzymes lipoprotein lipase and pancreatic lipase. ANGPTL4 is a potential target for ameliorating cardiometabolic diseases. Although ANGPTL4 has been implicated in obesity, the study of the direct role of ANGPTL4 in diet-induced obesity and related metabolic dysfunction is hampered by the massive acute-phase response and development of lethal chylous ascites and peritonitis in Angptl4 mice fed a standard high-fat diet. The aim of this study was to better characterise the role of ANGPTL4 in glucose homeostasis and metabolic dysfunction during obesity. METHODS: We chronically fed wild-type (WT) and Angptl4 mice a diet rich in unsaturated fatty acids and cholesterol, combined with fructose in drinking water, and studied metabolic function. The role of the gut microbiota was investigated by orally administering a mixture of antibiotics (ampicillin, neomycin, metronidazole). Glucose homeostasis was assessed via i.p. glucose and insulin tolerance tests. RESULTS: Mice lacking ANGPTL4 displayed an increase in body weight gain, visceral adipose tissue mass, visceral adipose tissue lipoprotein lipase activity and visceral adipose tissue inflammation compared with WT mice. However, they also unexpectedly had markedly improved glucose tolerance, which was accompanied by elevated insulin levels. Loss of ANGPTL4 did not affect glucose-stimulated insulin secretion in isolated pancreatic islets. Since the gut microbiota have been suggested to influence insulin secretion, and because ANGPTL4 has been proposed to link the gut microbiota to host metabolism, we hypothesised a potential role of the gut microbiota. Gut microbiota composition was significantly different between Angptl4 mice and WT mice. Interestingly, suppression of the gut microbiota using antibiotics largely abolished the differences in glucose tolerance and insulin levels between WT and Angptl4 mice. CONCLUSIONS/INTERPRETATION: Despite increasing visceral fat mass, inactivation of ANGPTL4 improves glucose tolerance, at least partly via a gut microbiota-dependent mechanism.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180304
[Lr] Last revision date:180304
[St] Status:Publisher
[do] DOI:10.1007/s00125-018-4583-5

  5 / 868 MEDLINE  
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[PMID]: 29311037
[Au] Autor:Boney A; Elser HE; Silver HJ
[Ti] Title:Relationships among Dietary Intakes and Persistent Gastrointestinal Symptoms in Patients Receiving Enzyme Treatment for Genetic Sucrase-Isomaltase Deficiency.
[So] Source:J Acad Nutr Diet;118(3):440-447, 2018 Mar.
[Is] ISSN:2212-2672
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Sucrose-isomaltase deficiency (SID) remains underdiagnosed. Absent or reduced enzyme activity promotes diarrhea, abdominal bloating, and flatulence from undigested and malabsorbed disaccharides. Frequency and severity of gastrointestinal symptoms may be associated with the type of carbohydrates consumed. OBJECTIVE: To characterize the dietary intakes of patients treated with sacrosidase (Sucraid; QOL Medical) for SID and determine relationships between type of carbohydrates, sacrosidase dose, and gastrointestinal symptoms. DESIGN: A prospective 30-day observational study. PARTICIPANTS/SETTING: Forty-nine patients treated with sacrosidase for ≥3 months were recruited from the enzyme manufacturer's nationwide clinical database between November 2014 and August 2015. MAIN OUTCOME MEASURES: Dietary energy and nutrient intakes reported during 24-hour diet recall interviews, frequency and severity of gastrointestinal (GI) symptoms, and sacrosidase dose. STATISTICAL ANALYSES PERFORMED: Relationships between nutrient intakes, sacrosidase dose, and GI symptoms were evaluated using Spearman ρ correlation coefficients. RESULTS: Sacrosidase dose averaged 5.2±3.1 mL/day. Participants reported 1.3±0.9 bowel movements daily. Having less frequent GI symptoms was associated with higher sacrosidase intake. Energy intakes averaged 1,562.5±411.5 kcal/day in children, 1,964.7±823.6 kcal/day in adolescents, and 1,952.6±546.5 kcal/day in adults. Macronutrient composition averaged 44% carbohydrate, 39% fat, and 17% protein. Average carbohydrate composition was 35% starch, 8% fiber, and 59% sugars. Sucrose and fructose intakes were not associated with GI symptoms. Lactose intake was associated with diarrhea. Maltose intake was associated with nausea, distension, and reflux. CONCLUSIONS: Intakes were lower in carbohydrates and higher in fat compared with the Acceptable Macronutrient Distribution Ranges. Sucrose and fructose intakes were not associated with GI symptoms. Higher maltose and lactose intakes were associated with GI symptom frequency and severity. These findings provide evidence to guide nutrition counseling for patients treated for SID.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180225
[Lr] Last revision date:180225
[St] Status:In-Data-Review

  6 / 868 MEDLINE  
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[PMID]: 29402406
[Au] Autor:Hayakawa M; Hira T; Nakamura M; Iida T; Kishimoto Y; Hara H
[Ad] Address:Graduate School of Agriculture, Hokkaido University, Sapporo 060-8589, Japan.
[Ti] Title:Secretion of GLP-1 but not GIP is potently stimulated by luminal d-Allulose (d-Psicose) in rats.
[So] Source:Biochem Biophys Res Commun;, 2018 Feb 02.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Glucagon-like peptide 1 (GLP-1), an incretin gastrointestinal hormone, is secreted when stimulated by nutrients including metabolizable sugars such as glucose and fructose. d-Allulose (allulose), also known as d-psicose, is a C-3 isomer of d-fructose and a rare sugar with anti-diabetic or anti-obese effects in animal models. In the present study, we examined whether an oral administration of allulose could stimulate GLP-1 secretion in rats, and investigated the underlying mechanisms. Oral, but not intraperitoneal, administration of allulose (0.5-2.0 g/kg body weight) elevated plasma GLP-1 levels for more than 2 h in a dose-dependent manner. The effects of allulose on GLP-1 secretion were higher than that of dextrin, fructose, or glucose. In addition, oral allulose increased total and active GLP-1, but not glucose-dependent insulinotropic polypeptide (GIP), levels in the portal vein. In anesthetized rats equipped with a portal catheter, luminal (duodenum and ileum) administration of allulose increased portal GLP-1 levels, indicating the luminal effect of allulose. Allulose-induced GLP-1 secretion was abolished in the presence of xanthohumol (a glucose/fructose transport inhibitor), but not in the presence of inhibitors of the sodium-dependent glucose cotransporter 1 or the sweet taste receptor. These results demonstrate a potent and lasting effect of orally administered allulose on GLP-1 secretion in rats, without affecting GIP secretion. The potent and selective GLP-1-releasing effect of allulose holds promise for the prevention and treatment of glucose intolerance through promoting endogenous GLP-1 secretion.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180206
[Lr] Last revision date:180206
[St] Status:Publisher

  7 / 868 MEDLINE  
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[PMID]: 29390242
[Au] Autor:Vigotti FN; Daidola G; Marciello A; Berruto F; Rizzuto A; Reina E; Perosa PM; Saltarelli M
[Ad] Address:S.S. Nefrologia e Dialisi, Ospedale E. Agnelli, Pinerolo, Turin, ASL TO3.
[Ti] Title:[Severe lactic acidosis requiring continuos haemodiafiltration in a young patient with unrecognized metabolic abnormality. Case report].
[So] Source:G Ital Nefrol;35(1), 2018 Feb.
[Is] ISSN:1724-5990
[Cp] Country of publication:Italy
[La] Language:ita
[Ab] Abstract:BACKGROUND: Lactic acidosis (LA) is the most common form of metabolic acidosis, defined by lactate values greater than 5 mmol/L and pH<7.34. The pathogenesis of LA involves hypoxic causes (type A) and non-hypoxic (type B), often coexisting. Identification and removal of the trigger are mandatory in the therapeutic management of LA. The case: A 38 years-old male patient entered the Emergency Ward for dyspnea, fever, vomiting and hyporexia. An important respiratory distress with hyperventilation due to severe LA was found, together with severe hypoglicemia, without renal impairment. Past medical history unremarkable, except for reported episodic hypoglicemia in the childhood, with fructose "intolerance", without any other data. No evidence of intoxications, septic shock or significant cytolysis. No drugs causing LA. The patient underwent orotracheal intubation, glucose infusion, and continuous haemodiafiltration for 36-hrs. A rapid general improvement was obtained with stabilization of acid-base balance. A diagnosis of fructose-1,6-diphosphatase deficiency was made. It is an autosomical recessive gluconeogenesis abnormality, with recurrent episodes of hypoglicemia and lactic acidosis after fasting, potentially lethal. The therapy is based on avoiding prolonged fasts, glucose infusion, and a specific diet, rich in glucose without fructose intake. CONCLUSIONS: The presence of not-otherwise-explained lactic acidosis in young patients has to place the suspect of an underlying and unknown metabolic derangement; in these cases, the involvement of the nephrologist appears to be pivotal for the differential diagnosis of the abnormalities of the acid-base balance, and for setting the best treatment.
[Pt] Publication type:CASE REPORTS; ENGLISH ABSTRACT
[Em] Entry month:1802
[Cu] Class update date: 180201
[Lr] Last revision date:180201
[St] Status:In-Process

  8 / 868 MEDLINE  
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[PMID]: 29250698
[Au] Autor:Pacurar D; Lesanu G; Dijmarescu I; Tincu IF; Gherghiceanu M; Oraseanu D
[Ad] Address:Emergency Department, "Grigore Alexandrescu" Emergency Hospital for Children, Bucharest, Romania; if_boian@yahoo.com.
[Ti] Title:Genetic disorder in carbohydrates metabolism: hereditary fructose intolerance associated with celiac disease.
[So] Source:Rom J Morphol Embryol;58(3):1109-1113, 2017.
[Is] ISSN:1220-0522
[Cp] Country of publication:Romania
[La] Language:eng
[Ab] Abstract:Celiac disease (CD) has been associated with several genetic and immune disorders, but association between CD and hereditary fructose intolerance (HFI) is extremely rare. HFI is an autosomal recessive disease caused by catalytic deficiency of aldolase B (fructose-1,6-bisphosphate aldolase). We report the case of a 5-year-old boy suffering from CD, admitted with an initial diagnosis of Reye's-like syndrome. He presented with episodic unconsciousness, seizures, hypoglycemia, hepatomegaly and abnormal liver function. The patient has been on an exclusion diet for three years, but he still had symptoms: stunting, hepatomegaly, high transaminases, but tissue transglutaminase antibodies were negative. Liver biopsy showed hepatic steatosis and mitochondrial damage. The dietary history showed an aversion to fruits, vegetables and sweet-tasting foods. The fructose tolerance test was positive, revealing the diagnostic of hereditary fructose intolerance. Appropriate dietary management and precautions were recommended. The patient has been symptom-free and exhibited normal growth and development until 10 years of age.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 171218
[Lr] Last revision date:171218
[St] Status:In-Process

  9 / 868 MEDLINE  
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[PMID]: 29117620
[Au] Autor:Wong SK; Chin KY; Suhaimi FH; Ahmad F; Ima-Nirwana S
[Ad] Address:Department of Pharmacology, Faculty of Medicine, Universiti Kebangsaan Malaysia, Jalan Yaakob Latif, Bandar Tun Razak, 56000 Cheras, Kuala Lumpur, Malaysia.
[Ti] Title:The Effects of a Modified High-carbohydrate High-fat Diet on Metabolic Syndrome Parameters in Male Rats.
[So] Source:Exp Clin Endocrinol Diabetes;, 2017 Nov 08.
[Is] ISSN:1439-3646
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:Metabolic syndrome is a cluster of metabolic abnormalities including central obesity, hyperglycemia, hypertension, and dyslipidemia. A previous study has established that high-carbohydrate high-fat diet (HCHF) can induce MetS in rats. In this study, we modified components of the diet so that it resembled the diet of Southeast Asians. This study aimed to determine the effects of this modified HCHF diet on metabolic parameters in rats. Male Wistar rats (n=14) were randomised into two groups. The normal group was given standard rat chow. The MetS group was given the HCHF diet, comprises of fructose, sweetened condensed milk, ghee, Hubble Mendel and Wakeman salt mixture, and powdered rat food. The diet regimen was assigned for a period of 16 weeks. Metabolic syndrome parameters (abdominal circumference, blood glucose, blood pressure, and lipid profile) were measured at week 0, 8, 12, and 16 of the study. The measurement of whole body composition (fat mass, lean mass, and percentage of fat) was performed using dual-energy X-ray absorptiometry at week 0, 8, and 16. Our results indicated that the components of MetS were partially developed after 8 weeks of HCHF diet. Systolic blood pressure, triglyceride, low density lipoprotein cholesterol, fat content, and percentage of fat was significantly higher in the HCHF group compared to normal group (p<0.05). After 12 weeks of HCHF diet, the rats showed significant increases in abdominal circumference, blood pressure, glucose intolerance, and dyslipidemia compared to normal control (p<0.05). In conclusion, MetS is successfully established in male rats induced by the modified HCHF diet after 12 weeks.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 171108
[Lr] Last revision date:171108
[St] Status:Publisher
[do] DOI:10.1055/s-0043-119352

  10 / 868 MEDLINE  
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Morais, Mauro Batista de
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[PMID]: 29111202
[Au] Autor:Ozaki RKF; Speridião PDGL; Soares ACF; Morais MB
[Ad] Address:Universidade Federal de São Paulo (UNIFESP), Escola Paulista de Medicina (EPM), Programa de Pós-graduação em Nutrição, São Paulo, SP, Brazil.
[Ti] Title:Intestinal fructose malabsorption is associated with increased lactulose fermentation in the intestinal lumen.
[So] Source:J Pediatr (Rio J);, 2017 Oct 28.
[Is] ISSN:1678-4782
[Cp] Country of publication:Brazil
[La] Language:eng
[Ab] Abstract:OBJECTIVE: To study fructose malabsorption in children and adolescents with abdominal pain associated with functional gastrointestinal disorders. As an additional objective, the association between intestinal fructose malabsorption and food intake, including the estimated fructose consumption, weight, height, and lactulose fermentability were also studied. METHODS: The study included 31 patients with abdominal pain (11 with functional dyspepsia, 10 with irritable bowel syndrome, and 10 with functional abdominal pain). The hydrogen breath test was used to investigate fructose malabsorption and lactulose fermentation in the intestinal lumen. Food consumption was assessed by food registry. Weight and height were measured. RESULTS: Fructose malabsorption was characterized in 21 (67.7%) patients (nine with irritable bowel syndrome, seven with functional abdominal pain, and five with functional dyspepsia). Intolerance after fructose administration was observed in six (28.6%) of the 21 patients with fructose malabsorption. Fructose malabsorption was associated with higher (p<0.05) hydrogen production after lactulose ingestion, higher (p<0.05) energy and carbohydrate consumption, and higher (p<0.05) body mass index z-score value for age. Median estimates of daily fructose intake by patients with and without fructose malabsorption were, respectively, 16.1 and 10.5g/day (p=0.087). CONCLUSION: Fructose malabsorption is associated with increased lactulose fermentability in the intestinal lumen. Body mass index was higher in patients with fructose malabsorption.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 171110
[Lr] Last revision date:171110
[St] Status:Publisher


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