26 research outputs found

    a randomized controlled trial

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    Diurnal carbohydrate and fat distribution modulates glycaemic control in rodents. In humans, the optimal timing of both macronutrients and its effects on glycaemic control after prolonged consumption are not studied in detail. In this cross-over trial, 29 non-obese men were randomized to two four-week diets: (1) carbohydrate-rich meals until 13.30 and fat-rich meals between 16.30 and 22.00 (HC/HF) versus (2) inverse sequence of meals (HF/HC). After each trial period two meal tolerance tests were performed, at 09.00 and 15.40, respectively, according to the previous intervention. On the HF/HC diet, whole-day glucose level was increased by 7.9% (p = 0.026) in subjects with impaired fasting glucose and/or impaired glucose tolerance (IFG/IGT, n = 11), and GLP-1 by 10.2% (p = 0.041) in normal glucose-tolerant subjects (NGT, n = 18). Diet effects on fasting GLP-1 (p = 0.009) and PYY (p = 0.034) levels were observed in IFG/IGT, but not in NGT. Afternoon decline of glucose tolerance was more pronounced in IFG/IGT and associated with a stronger decrease of postprandial GLP-1 and PYY levels, but not with changes of cortisol rhythm. In conclusion, the HF/HC diet shows an unfavourable effect on glycaemic control in IFG/IGT, but not in NGT subjects. Consequently, large, carbohydrate-rich dinners should be avoided, primarily by subjects with impaired glucose metabolism

    The effect of diurnal distribution of carbohydrates and fat on glycaemic control in humans: a randomized controlled trial.

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    Diurnal carbohydrate and fat distribution modulates glycaemic control in rodents. In humans, the optimal timing of both macronutrients and its effects on glycaemic control after prolonged consumption are not studied in detail. In this cross-over trial, 29 non-obese men were randomized to two four-week diets: (1) carbohydrate-rich meals until 13.30 and fat-rich meals between 16.30 and 22.00 (HC/HF) versus (2) inverse sequence of meals (HF/HC). After each trial period two meal tolerance tests were performed, at 09.00 and 15.40, respectively, according to the previous intervention. On the HF/HC diet, whole-day glucose level was increased by 7.9% (p = 0.026) in subjects with impaired fasting glucose and/or impaired glucose tolerance (IFG/IGT, n = 11), and GLP-1 by 10.2% (p = 0.041) in normal glucose-tolerant subjects (NGT, n = 18). Diet effects on fasting GLP-1 (p = 0.009) and PYY (p = 0.034) levels were observed in IFG/IGT, but not in NGT. Afternoon decline of glucose tolerance was more pronounced in IFG/IGT and associated with a stronger decrease of postprandial GLP-1 and PYY levels, but not with changes of cortisol rhythm. In conclusion, the HF/HC diet shows an unfavourable effect on glycaemic control in IFG/IGT, but not in NGT subjects. Consequently, large, carbohydrate-rich dinners should be avoided, primarily by subjects with impaired glucose metabolism

    Reduced postprandial energy expenditure and increased exogenous fat oxidation in young woman after ingestion of test meals with a low protein content

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    <p>Abstract</p> <p>Background</p> <p>Macronutrient composition of diets can influence energy balance in humans. We tested the hypothesis whether low protein content in single meals may induce lower values of energy expenditure (EE) and fat oxidation (FO) as compared to adequate protein content.</p> <p>Methods</p> <p>Indirect calorimetry was combined with a breath test using naturally <sup>13</sup>C-enriched corn oil to differentiate between postprandial exogenous and endogenous FO. Young women ingested single meals containing either 3.9% (low protein, LP) or 11.4% (adequate protein, AP) of total energy (~3100 kJ) as protein.</p> <p>Results</p> <p>Postprandial EE was 160 kJ/6 h lower (p < 0.01) after LP meals and diet induced thermogenesis (DIT) increased less (p < 0.001) as compared to AP meals. Total postprandial FO was not significantly different between meals (~17 g/6 h). However, exogenous postprandial FO was significantly (p < 0.01) higher (4.28 ± 1.57 g/6 h) after exposure to LP meals as compared to AP meals (1.87 ± 1.00 g/6 h). Less than 10% of ingested fat (50 g) was oxidized in the postprandial phase. The overall postprandial fat balance was approximately + 33 g.</p> <p>Conclusion</p> <p>Breath tests using naturally <sup>13</sup>C-labeled corn oil mirror exogenous FO. Low protein meals resulted in reduced postprandial EE and increased exogenous FO as compared to adequate protein meals without differences in total FO.</p

    Early Production of IL-22 but Not IL-17 by Peripheral Blood Mononuclear Cells Exposed to live Borrelia burgdorferi: The Role of Monocytes and Interleukin-1

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    If insufficiently treated, Lyme borreliosis can evolve into an inflammatory disorder affecting skin, joints, and the CNS. Early innate immunity may determine host responses targeting infection. Thus, we sought to characterize the immediate cytokine storm associated with exposure of PBMC to moderate levels of live Borrelia burgdorferi. Since Th17 cytokines are connected to host defense against extracellular bacteria, we focused on interleukin (IL)-17 and IL-22. Here, we report that, despite induction of inflammatory cytokines including IL-23, IL-17 remained barely detectable in response to B. burgdorferi. In contrast, T cell-dependent expression of IL-22 became evident within 10 h of exposure to the spirochetes. This dichotomy was unrelated to interferon-γ but to a large part dependent on caspase-1 and IL-1 bioactivity derived from monocytes. In fact, IL-1β as a single stimulus induced IL-22 but not IL-17. Neutrophils display antibacterial activity against B. burgdorferi, particularly when opsonized by antibodies. Since neutrophilic inflammation, indicative of IL-17 bioactivity, is scarcely observed in Erythema migrans, a manifestation of skin inflammation after infection, protective and antibacterial properties of IL-22 may close this gap and serve essential functions in the initial phase of spirochete infection

    Long term changes in the distribution and delta15N values of individual soil amino acids in the absence of plant and fertiliser inputs

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    International audienceThe long-term 'biodegradation' on soil amino acids was examined in the control plots of '42 parcelles' experiment, established in 1928 at INRA, Versailles (France). None of the plots is cultivated, but is kept free of weeds, and mixed to a depth of 25 cm twice yearly. Topsoil (0-10 cm depth) samples collected in 1929, 1963 and 1997 were subjected to acid hydrolysis (6 N HCl) for comparison. The distribution and delta15N natural abundance of 20 individual amino acids in the soils were determined, using ion chromatography (IC) and gas chromatography-combustion-isotope ratio mass spectrometry (GC-C-IRMS). The total N and amino acid-N (AA-N), respectively, decreased by 54 % and 73 % in the period from 1929 to 1997. The average N loss was comparable for 1929-1963 (period 1) and 1963-1997 (period 2), but AA-N loss was three times faster in the former period. This significant reduction in total AA-N content was mirrored in the individual amino acids, which decreased by 74 % ± 1 % (ranging 58-89 %) between 1929 and 1997. The bulk delta15N values generally increased from 1929 to 1997, mainly associated with comparable or even higher increase of delta15N of the non-AA-N in the soil. The residence time (t1/2, time in which half of N was lost from a specific soil pool) was ca. 65 ± 5 years for the bulk soil, and comparable for periods 1 and 2. However, between periods 1 and 2 it decreased from 128 to 41 years in the non-AA pool, but increased from 59 to 92 years in the AA-N pool. Proline and amino acids that appear early in soil microbial metabolic pathways (e.g. glutamic acid, alanine, aspartic acid and valine) had relatively high delta15N values. Phenylalanine, threonine, glycine and leucine had relatively depleted delta15N values. The average delta15N value of the individual amino acids (IAAs) increased by 1delta unit from 1929 to 1997, associated with a similar rise from 1929 to 1963, and no change thereafter till 1997. However, the delta15N values of phenylalanine decreased by more than 7delta15N units between 1929 and 1997. The delta15N shift of IAAs from 1929 to 1963 and from 1929 to 1997 was not influenced by the relative amount of N remaining compared with the 1929 soil concentrations. The only exception was phenylalanine which showed decreasing delta15N associated with its decreasing concentration in the soil. We conclude therefore that in the absence of plant and fertiliser inputs, no change in the delta15N value of individual soil amino acids occurs, hence the original delta15N values are preserved and diagnostic information on past soil N (cycling) is retained. The exception was phenylalanine, its delta15N decreased with decreasing concentration from 1929 to 1997, hence it acted as a 'potential' marker for the land use changes (i.e. arable cropping to a fallow). The long term biological processing and reworking of residual amino acids resulted in a (partial) stabilisation in the soil, evidenced by reduced N loss and increased residence time of amino acid N during the period 1963-199
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