Short-term alterations in carbohydrate energy intake in humans. Striking effects on hepatic glucose production, de novo lipogenesis, lipolysis, and whole-body fuel selection (original) (raw)
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Reduced oxidation of dietary fat after a short term high- carbohydrate diet1-3
2000
Background:Short-termhigh-carbohydrate(HC)dietsinducemet- abolic alterations, including hypertriacylglycerolemia, in both the fasting and postprandial states. The underlying tissue-specific alter- ations in fatty acid metabolism are not well understood. Objective: We investigated alterations in exogenous and endoge- nous fatty acid metabolism by using stable isotope tracers to label meal triacylglycerol and plasma fatty acids. Design:Eighthealthysubjectsconsumedisocaloricdietscontaining a high percentage of energy from carbohydrates or a
The Journal of Nutrition, 2021
Background Low-carbohydrate diets are suggested to exert metabolic benefits by reducing circulating triacylglycerol (TG) concentrations, possibly by enhancing mitochondrial activity. Objective We aimed to elucidate mechanisms by which dietary carbohydrate and fat differentially affect hepatic and circulating TG, and how these mechanisms relate to fatty acid composition. Methods Six-week-old, ∼300 g male Wistar rats were fed a high-carbohydrate, low-fat [HC; 61.3% of energy (E%) carbohydrate] or a low-carbohydrate, high-fat (HF; 63.5 E% fat) diet for 4 wk. Parameters of lipid metabolism and mitochondrial function were measured in plasma and liver, with fatty acid composition (GC), high-energy phosphates (HPLC), carnitine metabolites (HPLC-MS/MS), and hepatic gene expression (qPCR) as main outcomes. Results In HC-fed rats, plasma TG was double and hepatic TG 27% of that in HF-fed rats. The proportion of oleic acid (18:1n–9) was 60% higher after HF vs. HC feeding while the proportion o...
Hepatic gluconeogenic fluxes and glycogen turnover during fasting in humans. A stable isotope study
Journal of Clinical Investigation, 1997
Fluxes through intrahepatic glucose-producing metabolic pathways were measured in normal humans during overnight or prolonged (60 h) fasting. The glucuronate probe was used to measure the turnover and sources of hepatic UDP-glucose; mass isotopomer distribution analysis from [2-13 C 1 ]glycerol for gluconeogenesis and UDP-gluconeogenesis; [U-13 C 6 ]glucose for glucose production (GP) and the direct UDP-glucose pathway; and [1-2 H 1 ]galactose for UDP-glucose flux and retention in hepatic glycogen. After overnight fasting, GP (fluxes in milligram per kilogram per minute) was 2.19 Ϯ 0.09, of which 0.79 (36%) was from gluconeogenesis, 1.40 was from glycogenolysis, 0.30 was retained in glycogen via UDP-gluconeogenesis, and 0.17 entered hepatic UDP-glucose by the direct pathway. Thus, total flux through the gluconeogenic pathway (1.09) represented 54% of extrahepatic glucose disposal (2.02) and the net hepatic glycogen depletion rate was 0.93 (46%). Prolonging [2-13 C 1 ]glycerol infusion slowly increased measured fractional gluconeogenesis. In response to prolonged fasting, GP was lower (1.43 Ϯ 0.06) and fractional and absolute gluconeogenesis were higher (78 Ϯ 2% and 1.11 Ϯ 0.07, respectively). The small but nonzero glycogen input to plasma glucose (0.32 Ϯ 0.03) was completely balanced by retained UDPgluconeogenesis (0.31 Ϯ 0.02). Total gluconeogenic pathway flux therefore accounted for 99 Ϯ 2% of GP, but with a glycogen cycle interposed. Prolonging isotope infusion to 10 h increased measured fractional gluconeogenesis and UDP-gluconeogenesis to 84-96%, implying replacement of glycogen by gluconeogenic-labeled glucose. Moreover, after glucagon administration, GP (1.65), recovery of [1-2 H 1 ]galactose label in plasma glucose (25%) and fractional gluconeogenesis (91%) increased, such that 78% (0.45/0.59) of glycogen released was labeled (i.e., of recent gluconeogenic origin). In conclusion, hepatic gluconeogenic flux into glycogen and glycogen turnover persist during fasting in humans, reconciling inconsistencies in the literature and interposing another locus of control in the normal pathway of GP. (J.
European Journal of Clinical Nutrition, 2001
Objective: To determine dose-dependent relationship between ingested fat and its oxidation in the immediate post-prandial period in humans. Design: Subjects were randomly selected for the study at the Dunn Clinical Nutrition Centre, Cambridge, UK. Subjects ingested naturally enriched 13 C corn-oil doses (range 20 ± 140 g) in a whole-body indirect calorimeter, and were studied for 8 h. Ingested fat oxidation was estimated from the subject's breath 13 C enrichment and total carbon dioxide production. Total fat and carbohydrate oxidation were estimated from non-protein oxygen and carbon dioxide exchanges. Endogenous fat oxidation was estimated as the difference between total fat and ingested fat oxidation. Results: The amount of fat dose oxidized was nonlinearly related to the amount ingested. On average, 25.6 AE 2.7% of the mean fat dose was oxidized. A signi®cant (r 7 0.72, P`0.001) inverse correlation was found between the amount of fat dose and the proportion oxidized. Endogenous carbohydrate oxidation was negatively and signi®cantly correlated to fat dose oxidized (r 7 0.61, P`0.01), but it was not correlated to endogenous fat oxidation.
Diabetes, 2016
Resistance to the action of insulin affects fatty acid delivery to the liver, fatty acid synthesis and oxidation within the liver, and triglyceride export from the liver. To understand the metabolic consequences of hepatic fatty acid synthesis, partitioning, oxidation, and net liver fat content in the fasted and postprandial states, we used stable-isotope tracer methodologies to study healthy men and women with varying degrees of insulin resistance before and after consumption of a mixed meal. Subjects were classified as being normoinsulinemic (NI) (fasting plasma insulin <11.2 mU/L, n = 18) or hyperinsulinemic (HI) (fasting plasma insulin >11.2 mU/L, n = 19). Liver fat content was similar between HI and NI individuals, despite HI subjects having marginally more visceral fat. However, de novo lipogenesis was higher and fatty acid oxidation was lower in HI individuals compared with NI subjects. These data suggest that metabolic pathways promoting fat accumulation are enhanced i...
British Journal of Nutrition, 1980
1. Total carbohydrate (CHO) and ingested glucose oxidation was measured in five obese subjects with normal glucose tolerance after an oral load of 100g naturally-labelled [13C]glucose using indirect calorimetry and mass spectrometry respectively.2. CHO utilization rate (107 ± 14 mg/min in the post-absorptive state) increased 30 min after the glucose load to reach a plateau (245±25 mg/min) between 90 and 120 min. It then decreased to basal values at 330 min. Cumulative CHO oxidation over 480 min was 66±7 g and the CHO oxidized above basal levels was 26 ± 7g.3. Enrichment of expired carbon dioxide with 13c began at 45 min and maximum values were observed between 210 and 300 min. At 480 min, cumulative oxidation of the ingested glucose was 24± 2 g.4. Compared with controls, the obese subjects exhibit an impairment of CHO utilization which precedes glucose intolerance. This impairment can be explained by an increased availability of free fatty acids which favours lipid oxidation at the ...
Critical Reviews in Food Science and Nutrition, 2014
Aim: The purpose of this review was to assess existing evidence on the effects of chronic dietary macronutrient composition on substrate oxidation during a fasted state in healthy and overweight subjects. Methods: A systematic review of studies was conducted across five databases. Studies were included if they were English language studies of human adults, 19 years, used indirect calorimetry (ventilated hood technique), specified dietary macronutrient composition and measured substrate oxidation. Results: There was no evidence that variations of a typical, non-experimental diet influenced rate or ratio of substrate utilisation, however there may be an upper and lower threshold for when macronutrient composition may directly alter preferences for fuel oxidation rates during a fasted state. Conclusion: This review indicates that macronutrient composition of a wide range of typical, nonexperimental dietary fat and carbohydrate intakes has no effect on fasting substrate oxidation. This suggests that strict control of dietary intake prior to fasting indirect calorimetry measurements may be an unnecessary burden for study participants. Further research into the effects of long-term changes in isocaloric macronutrient shift is required.
Dietary Energy Partition: The Central Role of Glucose
International Journal of Molecular Sciences
Humans have developed effective survival mechanisms under conditions of nutrient (and energy) scarcity. Nevertheless, today, most humans face a quite different situation: excess of nutrients, especially those high in amino-nitrogen and energy (largely fat). The lack of mechanisms to prevent energy overload and the effective persistence of the mechanisms hoarding key nutrients such as amino acids has resulted in deep disorders of substrate handling. There is too often a massive untreatable accumulation of body fat in the presence of severe metabolic disorders of energy utilization and disposal, which become chronic and go much beyond the most obvious problems: diabetes, circulatory, renal and nervous disorders included loosely within the metabolic syndrome. We lack basic knowledge on diet nutrient dynamics at the tissue-cell metabolism level, and this adds to widely used medical procedures lacking sufficient scientific support, with limited or nil success. In the present longitudinal...
British Journal of Nutrition, 1979
1. Carbohydrate (CHO) oxidation was measured simultaneously in a group of five normal subjects after an oral load of 100 g naturally-labelled [13C]glucose, using indirect calorimetry and mass spectrometry.2. CHO utilization, calculated from the results of indirect calorimetry, increased 30 min after the glucose load to reach a peak at 90 min. It then decreased to reach basal values at 380 min. Cumulative total CHO oxidation at 480 min was 83±8g, and CHO oxidized above basal levels, 37±3 g.3. Enrichment of expired carbon dioxide with13C began at 60 min and maximum values were observed at 270 min. At 480 min, cumulative CHO oxidation measured by use of [13C]glucose was 29 g. The difference from calorimetric values can be attributed in part to the slow isotopic dilution in the glucose and bicarbonate pools.4. Thus, approximately 30% of the glucose load was oxidized during the 8 h after its ingestion and this accounts for a significant part of the increased CHO oxidation (37 g), as meas...