Fecal fat excretion. An analysis of four years' experience

1967 ◽  
Vol 119 (6) ◽  
pp. 573-576 ◽  
Author(s):  
E. C. Raffensperger
Keyword(s):  
Fecal Fat ◽  
Fat Excretion

Stimulation of fecal fat excretion and the disposal of protoporphyrin in a murine model for erythropoietic protoporphyria

2007 ◽  
Vol 293 (2) ◽  
pp. G510-G516
Author(s):  
Karin E. R. Gooijert ◽  
Rick Havinga ◽  
Alida R. Oosterloo-Duinkerken ◽  
Enge E. A. Venekamp-Hoolsema ◽  
Folkert Kuipers ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Fecal Excretion ◽  
High Fat ◽  
Erythropoietic Protoporphyria ◽  
Low Fat Diet ◽  
Fecal Fat ◽  
Sucrose Polyesters ◽  
Hydrophobic Compound ◽  
Fat Excretion ◽  
Stimulation Of

Erythropoietic protoporphyria (EPP) is characterized by toxic accumulation of the hydrophobic compound protoporphyrin (PP). Ferrochelatase-deficient ( fch/ fch) mice are an animal model for human EPP. Recently, we have demonstrated that the accumulation of another hydrophobic compound, unconjugated bilirubin, could effectively be treated by stimulation of fecal fat excretion. We investigated whether stimulation of fecal fat excretion enhanced the disposal of PP in fch/ fch mice. Fch/ fch mice were fed for 8 wk with a high-fat diet (16 wt% fat; control) or with the high-fat diet mixed with either a nonabsorbable fat (sucrose polyester) or the intestinal lipase inhibitor orlistat. The effects of the treatments on fecal excretion of fat and PP and on hepatic PP concentrations were compared with control diets. Fecal fat excretion in fch/ fch mice on a high-fat diet was higher than in mice on a low-fat diet (+149%, P < 0.05). Sucrose polyesters and orlistat increased fecal fat excretion even more, up to sixfold of control values. However, none of the different treatments affected fecal PP excretion or hepatic PP concentration. Treatment of fch/ fch mice with a high-fat diet, a nonabsorbable fat diet, or with orlistat increased the fecal excretion of fat but did not increase fecal PP excretion or decrease hepatic PP concentration. The present data indicate that accumulation of PP is not amenable to stimulation of fecal fat excretion.

scholarly journals Effect of dairy calcium from cheese and milk on fecal fat excretion, blood lipids, and appetite in young men

2014 ◽  
Vol 99 (5) ◽  
pp. 984-991 ◽  
Author(s):  
Karina V Soerensen ◽  
Tanja K Thorning ◽  
Arne Astrup ◽  
Mette Kristensen ◽  
Janne K Lorenzen
Keyword(s):  
Blood Lipids ◽  
Young Men ◽  
Fecal Fat ◽  
Fat Excretion

scholarly journals Elimination of 72-Hour Quantitative Fecal Fat Testing by Restriction, Laboratory Consultation, and Evaluation of Specimen Weight and Fat Globules

2018 ◽  
Vol 3 (3) ◽  
pp. 357-365
Author(s):  
Michael Korostensky ◽  
Steven R Martin ◽  
Mark Swain ◽  
Maitreyi Raman ◽  
Christopher T Naugler ◽  
...  
Keyword(s):  
Roc Curves ◽  
Geographic Region ◽  
Discrimination Power ◽  
Fat Globules ◽  
Fecal Fat ◽  
Southern Alberta ◽  
Specimen Weight ◽  
Qualitative Test ◽  
Fat Excretion ◽  
Clinical Biochemist

Abstract Background The 72-h quantitative fecal fat test has been mostly obsolete for many years. Our objective was to reduce and eliminate the use of this test, while providing suitable alternatives. Methods We assessed (2010–2016) utilization of the fecal fat test in Calgary, Central Alberta, and Southern Alberta, Canada. Alternatives were identified through literature review and consultation with gastroenterologist stakeholders. Logistic regression and ROC curves were used to characterize discrimination power of 72-h specimen weight on abnormal fat excretion. This was also examined in 91 subspecimens that were additionally tested for the presence of fat globules. Results As 69% of fecal fat tests (total, 106/year) were on adults (age ≥ 18), stakeholders agreed that adult specimens should not be tested until ordering physicians consulted with a clinical biochemist. This change reduced fecal fat testing by 81% to 20/year in 2015. The 72-h specimen weight was a significant predictor of abnormal fat excretion [P &lt; 0.001; area under curve (AUC) = 0.75–0.79, n = 115–417] in historic fecal fat data. A similar result was observed among subspecimens (AUC = 0.70), which improved when additionally considering the presence of fat globules (AUC = 0.74). Stakeholders consented to replacing fecal fat with a comparison of specimen weight to cutpoints with 80% specificity for abnormal fat excretion, and the test for fat globules. Conclusion Through stakeholder engagement, we implemented changes that eliminated 72-h quantitative fecal fat testing in a large geographic region in Alberta, Canada. Future fecal fat orders would be reflexed to an assessment of 72-h specimen weight and a qualitative test for fat globules in stool.

scholarly journals Effect of silk powder from Bombyx mori or Antheraeapernyi on defecation and fecal fat excretion in rats

2014 ◽  
Vol 25 (3) ◽  
pp. 185-190 ◽  
Author(s):  
Ken-ichi Kobayashi ◽  
Yu Matsumoto ◽  
Misato Hirota ◽  
Takahumi Enda ◽  
Akiko Teramoto ◽  
...  
Keyword(s):  
Bombyx Mori ◽  
Fecal Fat ◽  
Fat Excretion

Fecal fat excretion in irritable bowel syndrome

2012 ◽  
Vol 47 (8-9) ◽  
pp. 1120-1121 ◽  
Author(s):  
Arnold Berstad ◽  
Mette Helvik Morken ◽  
Gülen Arslan Lied ◽  
Ragna Lind ◽  
Aud-Sissel Hjartholm ◽  
...  
Keyword(s):  
Irritable Bowel Syndrome ◽  
Fecal Fat ◽  
Irritable Bowel ◽  
Fat Excretion

Role of CCK in regulation of pancreaticobiliary functions and GI motility in humans: effects of loxiglumide

1991 ◽  
Vol 260 (2) ◽  
pp. G197-G206 ◽  
Author(s):  
W. E. Schmidt ◽  
W. Creutzfeldt ◽  
A. Schleser ◽  
A. R. Choudhury ◽  
R. Nustede ◽  
...  
Keyword(s):  
Pancreatic Enzyme ◽  
Enzyme Secretion ◽  
Gallbladder Contraction ◽  
Stool Weight ◽  
Gallbladder Volume ◽  
Fecal Fat ◽  
Pancreatic Enzyme Secretion ◽  
Fat Excretion ◽  
Gi Motility

To evaluate the physiological role of cholecystokinin (CCK) in humans, we studied the influence of the specific CCK receptor antagonist loxiglumide (CR 1505) on gallbladder contraction, pancreatic enzyme output, plasma CCK concentrations, mouth-to-cecum transit time (MCTT), stool weight, and fecal fat excretion. Infusion of CCK-8, producing CCK plasma levels of 10-12 pmol/l, decreased gallbladder volume to 21% of the initial volume (P less than 0.01) and increased bilirubin output 8- to 10-fold and pancreatic enzyme secretion 2- to 4-fold. Infusion of loxiglumide (10 mg.kg-1.h-1 iv) abolished CCK-8-stimulated enzyme and bilirubin output. Basal gallbladder volume increased 68% during loxiglumide infusion (P less than 0.001) and 137% (P less than 0.001) after 7 days of oral loxiglumide treatment (3 x 1.6 g/day). Gallbladder contraction and bilirubin output in response to the intraduodenal instillation of a liquid meal (382 kcal) was completely inhibited by loxiglumide; gallbladder volume even increased 45% postprandially during loxiglumide infusion (P less than 0.02) and 145% after long-term loxiglumide treatment (P less than 0.001). Meal-stimulated pancreatic enzyme output was diminished 46-53% after acute and 25-29% after chronic administration of loxiglumide. Meal-stimulated integrated plasma CCK-immunoreactive (CCK-ir) concentrations, determined by RIA, were 3.2-fold higher during loxiglumide infusion (P less than 0.02); plateau CCK levels were markedly elevated (10.1 +/- 1.4 vs. 3.7 +/- 0.5 pM). Plasma CCK-like bioactivity, measured by a sensitive bioassay, was identical to CCK-ir levels in the absence of loxiglumide; in the presence of loxiglumide, no circulating CCK-like bioactivity was detectable, indicating complete inhibition of plasma CCK. MCTT was augmented 24% (P less than 0.05). Oral treatment with loxiglumide increased stool weight 72% (P less than 0.01) and fecal fat excretion 186% (P less than 0.001). In conclusion, 1) meal-induced gallbladder contraction and fasting tone are primarily controlled by CCK; 2) the contribution of CCK to the intestinal phase of postprandial pancreatic enzyme secretion is 40-50%; 3) GI motility and absorption are partially controlled by CCK; and 4) postprandial CCK secretion is substantially augmented by loxiglumide via an unknown mechanism.

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