Ingestion of pure fructose stimulates de novo lipogenesis and gluconeogenesis. This may however not be relevant to typical nutritional situations, where fructose is invariably ingested with glucose. We therefore assessed the metabolic fate of fructose incorporated in a mixed meal without or with glucose in eight healthy volunteers. Each participant was studied over six hours after the ingestion of liquid meals containing either 13C-labelled fructose, unlabeled glucose, lipids and protein (Fr + G) or 13C-labelled fructose, lipids and protein, but without glucose (Fr), or protein and lipids alone (ProLip). After Fr + G, plasma 13C-glucose production accounted for 19.0% ± 1.5% and 13CO2 production for 32.2% ± 1.3% of 13C-fructose carbons. After Fr, 13C-glucose production (26.5% ± 1.4%) and 13CO2 production (36.6% ± 1.9%) were higher (p < 0.05) than with Fr + G. 13C-lactate concentration and very low density lipoprotein VLDL 13C-palmitate concentrations increased to the same extent with Fr + G and Fr, while chylomicron 13C-palmitate tended to increase more with Fr + G. These data indicate that gluconeogenesis, lactic acid production and both intestinal and hepatic de novo lipogenesis contributed to the disposal of fructose carbons ingested together with a mixed meal. Co-ingestion of glucose decreased fructose oxidation and gluconeogenesis and tended to increase 13C-pamitate concentration in gut-derived chylomicrons, but not in hepatic-borne VLDL-triacylglycerol (TG). This trial was approved by clinicaltrial. gov. Identifier is NCT01792089.
Polyneuropathy has been reported in cerebrotendinous xanthomatosis (CTX), although its nature and possible association with certain genotypes and phenotypes are unclear. The effect of chronic administration of chenodeoxycholic acid (CDCA) on peripheral nerve conduction parameters is still debated. We report clinical, laboratory, and electrophysiological findings in 35 CTX patients. Twenty-six subjects (74.2 %) showed peripheral nerve abnormalities. Polyneuropathy was predominantly axonal (76.9 % of patients) and generally mild. No correlation was found between its presence and clinical or biochemical data. In polyneuropathic patients, CDCA treatment improved electrophysiological conduction parameters, irrespective of the duration of therapy. Improvement mainly concerned nerve conduction velocities, whereas most nerve amplitudes remained unchanged. This means that CDCA treatment did not influence the number of axons activated by maximum electrical stimulation but increased the conduction of the still-excitable fibers. Our findings may suggest that CDCA treatment promotes myelin synthesis in nerve fibers with residual unaffected axons. The effect of therapy may therefore depend largely on the extent of irreversible structural damage to axons.
Objective: Fructose is partly metabolized in small bowel enterocytes, where it can be converted into glucose or fatty acids. It was therefore hypothesized that Roux-en-Y gastric bypass (RYGB) may significantly alter fructose metabolism. Methods: We performed a randomized clinical study in eight patients 12-17 months after RYGB and eight control (Ctrl) subjects. Each participant was studied after ingestion of a protein and lipid meal (PL) and after ingestion of a protein1lipid1fructose1glucose meal labeled with 13 C-fructose (PLFG). Postprandial blood glucose, fructose, lactate, apolipoprotein B48 (apoB48), and triglyceride (TG) concentrations, 13 C-palmitate concentrations in chylomicron-TG and VLDL-TG, fructose oxidation ( 13 CO 2 production), and gluconeogenesis from fructose (GNGf) were measured over 6 hours. Results: After ingestion of PLFG, postprandial plasma fructose, glucose, insulin, and lactate concentrations increased earlier and reached higher peak values in RYGB than in Ctrl. GNGf was 33% lower in RYGB than Ctrl (P 5 0.041), while fructose oxidation was unchanged. Postprandial incremental areas under the curves for total TG and chylomicrons-TG were 72% and 91% lower in RYGB than Ctrl (P 5 0.064 and P 5 0.024, respectively). ApoB48 and 13 C-palmitate concentrations were not significantly different. Conclusions: Postprandial fructose metabolism was not grossly altered, but postprandial lipid concentrations were markedly decreased in subjects having had RYGB surgery.
This article is available online at http://www.jlr.org Dietary fats are not only a source of energy, but also of bioactive nutrients, which are essential in maintaining human health. Among the fats, some FAs are considered essential FAs (EFAs) because they are not de novo synthesized and humans lack the enzymes required for their biosynthesis. Dietary fat absorption involves two main steps: first, lipolysis of dietary triacylglycerol (TAG) by sn-1,3' specific gastric and (colipase-dependent) pancreatic lipases to release two FFAs, and an sn-2 monoacylglycerol (MAG); and second, the formation of micellar structures (via association of intraluminal conjugated bile salts and lipolytic products), which aid enteral uptake (1, 2). Conventional knowledge indicates that FAs at the sn-1 and -3 positions are hydrolyzed and sn-2 FA is absorbed directly as monoglycerides; as such, the stereospecific position of FAs on the TAG backbone plays an important role in determining the uptake and metabolic fate of a particular FA (especially EFA) (1, 3). FAs such as linoleic acid (LA) and -linolenic acid (ALA) are EFAs, and dietary ALA can be metabolically converted to other long-chain PUFAs (LC-PUFAs), such as DHA and EPA, with recognized beneficial health effects. However, the efficiency of enzymatic conversion from ALA to DHA/EPA appears to be relatively low in humans (4). Therefore, larger quantities of DHA/EPA may be obtained from dietary sources such as fatty fish for ultimate health benefit. Among their health benefits, EPA and DHA are cardioprotective and have a positive impact on inflammatory conditions by interfering with the production of systemic inflammatory mediators, such as leukotrienes, platelet-activating factor, interleukin-l, and tumor necrosis factor (5-7). Impairment of intestinal uptake of fat in
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