Track topics on Twitter Track topics that are important to you
Excessive consumption of sweets is a risk factor for metabolic syndrome. A major chemical feature of sweets is fructose. Despite strong ties between fructose and disease, the metabolic fate of fructose in mammals remains incompletely understood. Here we use isotope tracing and mass spectrometry to track the fate of glucose and fructose carbons in vivo, finding that dietary fructose is cleared by the small intestine. Clearance requires the fructose-phosphorylating enzyme ketohexokinase. Low doses of fructose are ∼90% cleared by the intestine, with only trace fructose but extensive fructose-derived glucose, lactate, and glycerate found in the portal blood. High doses of fructose (≥1 g/kg) overwhelm intestinal fructose absorption and clearance, resulting in fructose reaching both the liver and colonic microbiota. Intestinal fructose clearance is augmented both by prior exposure to fructose and by feeding. We propose that the small intestine shields the liver from otherwise toxic fructose exposure.
This article was published in the following journal.
Name: Cell metabolism
Fructose consumption has increased due to widespread use of high-fructose corn syrup by the food industry. Renal proximal tubules are thought to reabsorb fructose. However, fructose reabsorption (J) b...
Dietary macronutrient composition alters metabolism through several mechanisms, including post-translational modification (PTM) of proteins. To connect diet and molecular changes, here we performed sh...
Dietary fructose is a major contributor to the epidemic of diabetes and obesity, and it is an excellent model to study metabolic syndrome. Based on previous studies that Bgn gene occupies a central po...
The sugar content of the tomato fruit is a primary determinant of taste and quality. Cultivated tomato fruit are characterized by near equimolar levels of the hexoses, glucose and fructose, derived fr...
Exon-skipping antisense oligonucleotides (AOs) are promising treatments for muscle-related genetic ailments including Duchenne muscular dystrophy (DMD), but clinical translation is unfortunately hampe...
This study is designed to test the effects on liver fat of varying fat intake in the presence of fructose or glucose. We hypothesize that higher dietary fat when eaten with fructose as com...
Dietary fructose potently exacerbates the dyslipidemia associated with obesity, insulin resistance and accelerated atherosclerosis. In a randomized crossover outpatient study of 15 overwei...
Non alcoholic fatty liver disease (NAFLD) is the most common cause of abnormal liver function tests in the U.S. (Browning, et al., 2004), ranging from steatosis to end-stage liver disease....
The increasing intake of fructose has been associated with an increase in obesity among US children and adolescents, but its "dose dependent" effects on insulin sensitivity and lipid metab...
In the U.S., dietary fructose has increased in parallel with the increase in obesity and may promote the development of diabetes and other chronic diseases. The largest source of dietary f...
A hexose transporter that mediates FRUCTOSE transport in SKELETAL MUSCLE and ADIPOCYTES and is responsible for luminal uptake of dietary fructose in the SMALL INTESTINE.
The founding member of the sodium glucose transport proteins. It is predominately expressed in the INTESTINAL MUCOSA of the SMALL INTESTINE.
An ester of glucose with phosphoric acid, made in the course of glucose metabolism by mammalian and other cells. It is a normal constituent of resting muscle and probably is in constant equilibrium with fructose-6-phosphate. (Stedman, 26th ed)
A metabolic process that converts GLUCOSE into two molecules of PYRUVIC ACID through a series of enzymatic reactions. Energy generated by this process is conserved in two molecules of ATP. Glycolysis is the universal catabolic pathway for glucose, free glucose, or glucose derived from complex CARBOHYDRATES, such as GLYCOGEN and STARCH.
An autosomal recessive fructose metabolism disorder due to deficient fructose-1-phosphate aldolase (EC 220.127.116.11) activity, resulting in accumulation of fructose-1-phosphate. The accumulated fructose-1-phosphate inhibits glycogenolysis and gluconeogenesis, causing severe hypoglycemia following ingestion of fructose. Prolonged fructose ingestion in infants leads ultimately to hepatic failure and death. Patients develop a strong distaste for sweet food, and avoid a chronic course of the disease by remaining on a fructose- and sucrose-free diet.
Enzymes are proteins that catalyze (i.e., increase the rates of) chemical reactions. In enzymatic reactions, the molecules at the beginning of the process, called substrates, are converted into different molecules, called products. Almost all chemical re...
Hepatology is the study of liver, gallbladder, biliary tree, and pancreas, and diseases associated with them. This includes viral hepatitis, alcohol damage, cirrhosis and cancer. As modern lifestyles change, with alcoholism and cancer becoming more promi...