Related Experiment Video
Updated: Jul 18, 2026

28:15
Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
Published on: July 28, 2010
Hyperoxaluria correlates with fat malabsorption in patients with sprue
Gut
|July 1, 1977
Summary
Severe fat malabsorption, common in sprue, can cause hyperoxaluria (high urinary oxalate). Improving fat absorption through dietary changes, like restricting gluten for coeliac sprue, reduced oxalate excretion in patients.
Area of Science:
- Gastroenterology
- Nephrology
- Nutritional Science
Background:
- Fat malabsorption is linked to various gastrointestinal disorders.
- Enteric hyperoxaluria is a condition characterized by elevated urinary oxalate levels.
- The precise relationship between fat malabsorption and oxalate excretion requires further elucidation.
Purpose of the Study:
- To investigate the impact of fat malabsorption on dietary oxalate absorption and renal excretion.
- To determine the correlation between the severity of fat malabsorption and urinary oxalate levels.
- To assess the effect of improved fat absorption on hyperoxaluria in patients with sprue.
Main Methods:
- Studied four patients with sprue and two with dermatitis herpetiformis and sprue-like histology.
- Monitored urinary oxalate excretion in relation to fat malabsorption.
- Analyzed fecal fat content and its correlation with urinary oxalate levels.
- Observed changes in urinary oxalate following dietary gluten restriction.
Main Results:
- Hyperoxaluria was present in all sprue patients with severe fat malabsorption.
- Urinary oxalate decreased in coeliac sprue patients after gluten restriction improved fat absorption.
- Patients with dermatitis herpetiformis and sprue, without steatorrhoea, had normal urinary oxalate.
- A significant positive linear relationship (r=0.82) was found between fecal fat and urinary oxalate.
Conclusions:
- Severe fat malabsorption plays a primary role in causing enteric hyperoxaluria.
- Dietary fat malabsorption is a key factor contributing to elevated oxalate levels in the gut.
- Managing fat malabsorption may be crucial for controlling hyperoxaluria in susceptible individuals.
More Related Videos
Related Concept Videos
Lethal Alleles
Agouti: A Lethal Allele
Lucien Cuénot discovered lethal alleles in 1905 while studying the inheritance of coat color in mice. The agouti gene is responsible for the color of the coat in mice. This gene codes for an agouti-signaling protein, which is responsible for melanin distribution in mammals. The wild-type allele gives rise to gray-brown coat color in mice, while the mutant allele gives rise to yellow coat color. In addition to coat color, the agouti gene is associated with the yellow...
Lucien Cuénot discovered lethal alleles in 1905 while studying the inheritance of coat color in mice. The agouti gene is responsible for the color of the coat in mice. This gene codes for an agouti-signaling protein, which is responsible for melanin distribution in mammals. The wild-type allele gives rise to gray-brown coat color in mice, while the mutant allele gives rise to yellow coat color. In addition to coat color, the agouti gene is associated with the yellow...
Protein Import into the Peroxisomes
Cells contain membrane-bound organelles called peroxisomes that oxidize organic molecules by transferring hydrogen atoms to oxygen, producing hydrogen peroxide. Peroxisomes enzymatically convert the released hydrogen peroxide into water and oxygen.
Peroxisomal Protein Import:
Peroxisomes lack the genetic machinery required to code for their own proteins. Hence, most peroxisomal membrane, lumenal and transmembrane proteins are synthesized in the cytoplasm or ER and transported to the peroxisome...
Peroxisomal Protein Import:
Peroxisomes lack the genetic machinery required to code for their own proteins. Hence, most peroxisomal membrane, lumenal and transmembrane proteins are synthesized in the cytoplasm or ER and transported to the peroxisome...
Inborn Errors of Metabolism
Phenylketonuria (PKU) is a protein metabolism disorder characterized by high blood levels of the amino acid phenylalanine. This results from a mutation in the gene responsible for phenylalanine hydroxylase, an enzyme that converts phenylalanine into tyrosine. When this enzyme is deficient, phenylalanine builds up in the blood, leading to symptoms such as vomiting, rashes, seizures, growth deficiency, and severe mental retardation. An early diagnosis and a diet restricting phenylalanine intake...
Peptic Ulcer Disease I: Introduction
Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
Peptic Ulcer
Peptic ulcers are erosive lesions of the gastric or duodenal lining, most commonly caused by Helicobacter pylori infection. This Gram-negative, helical bacterium has adapted to survive the stomach’s acidic environment by producing urease, which converts urea into ammonia and carbon dioxide. The ammonia neutralizes gastric acid in the bacterium’s immediate environment, allowing colonization of the gastric mucosa. H. pylori attaches to mucus-secreting epithelial cells, penetrates the mucus...
Pyloric Obstruction
Pyloric obstruction, also referred to as gastric outlet obstruction, is a condition characterized by narrowing or blockage at the pylorus—the muscular valve regulating the flow of stomach contents into the duodenum. When this passage becomes impaired, the stomach cannot effectively empty its contents into the small intestine. This disruption leads to a range of gastrointestinal symptoms, including early satiety, bloating, epigastric pain, postprandial nausea, persistent vomiting, and...

