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Effect of postprandial modulation of glucose availability: short- and long-term analysis
- Julie-Anne Nazare, Alexis de Rougemont, Sylvie Normand, Valérie Sauvinet, Monique Sothier, Sophie Vinoy, Michel Désage, Martine Laville
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- Journal:
- British Journal of Nutrition / Volume 103 / Issue 10 / 28 May 2010
- Published online by Cambridge University Press:
- 24 December 2009, pp. 1461-1470
- Print publication:
- 28 May 2010
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Low glycaemic index (LGI) foods have been proposed as potential means to decrease postprandial glucose excursions and thus to improve diabetes management. We modulated glucose availability of cereal products and thus their glycaemic index to study the metabolic effect of LGI foods on daylong glucose control acutely and in the long term following a 5-week GI intervention diet in free-living subjects. In this randomised, parallel trial, two groups of nineteen overweight subjects followed an ad libitum 5-week intervention diet in which usual starch was replaced by either LGI or high GI (HGI) starch. During the exploration days (days 1 and 36), subjects ate their assigned 13C-labelled test breakfast (LGI or HGI), and total and exogenous glucose kinetics (using stable isotopes), postprandial concentrations of glucose, insulin, lipid profile and nutrient oxidation were assessed after the test breakfast and a standardised lunch. At day 1, LGI breakfast significantly decreased post-breakfast glycaemic response with a parallel decrease in exogenous and total glucose appearance (P < 0·05). Post-lunch and post-breakfast glycaemic responses were positively correlated (r 0·79, P < 0·0001). Following the 5-week diet, difference between the groups in terms of glucose kinetics and response was maintained (no significant interaction group × time) but tended to decrease over time for the post-breakfast glycaemic response. Post-lunch and post-breakfast glycaemic responses remained positively correlated (r 0·47, P = 0·004). Modulation of postprandial glucose availability at breakfast decreased plasma exogenous glucose appearance and improved glucose control at the subsequent lunch. After 5 weeks, these effects were maintained in healthy subjects but remained to be confirmed in the longer term.
Oxidative stress in primiparous cows in relation to dietary starch and the progress of lactation
- G. Gabai, S. Testoni, R. Piccinini, L. Marinelli, C. M. Howard, G. Stradaioli
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- Journal:
- Animal Science / Volume 79 / Issue 1 / August 2004
- Published online by Cambridge University Press:
- 18 August 2016, pp. 99-108
- Print publication:
- August 2004
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Oxidative stress may be important in early lactation cows due to high metabolic demands. Modifying dietary starch may alter glucose utilization, modify oxidative metabolism and, consequently, increase oxidative stress. To test this hypothesis, early lactation primiparous cows underwent a short-term dietary starch restriction followed by realimentation. At calving, 10 Friesian primiparous cows were randomly assigned to two groups and given a basal starch diet (BSD, 249 g/kg of starch dry matter (DM)) in the form of a total mixed ration until 42 days in milk (DIM). Afterwards, five cows (CTR) continued to receive the same diet and five cows (EXP) were allotted to experimental diets: low starch diet (LSD, 210 g/kg starch DM) from 43 to 65 DIM followed by high starch diet (HSD, 283 g/kg starch DM) from 66 to 85 DIM and BSD from 86 to 94 DIM. Blood samples were collected at 37, 50, 60, 70, 80, and 94 DIM to measure total plasma glutathione (GSH), thiobarbituric acid reactive substances (TBARS), and erythrocyte glutathione peroxidase (GPx) activity as indicators of oxidative stress, N-acetyl-ß-D glucosaminidase (NAGase), lysosyme, and white blood cell counts as indicators of immune response. Metabolic adaptations were evaluated by glucose, non-esterified fatty acids (NEFA), beta-hydroxy-butyrate (BOHB), insulin, and GH concentrations, and the acid/base balance. Milk yield was not significantly different between groups throughout the experiment and was correlated with TBARS (r 0·284; P 0·05) and GSH (r = 0·294; P 0·05). Estimated energy intake was significantly higher in the EXP group at 70 DIM only (P 0·05). Plasma glucose was significantly lower in the EXP group at 50, 60 (P 0·001) and 80 DIM (P 0·05), and was correlated with GSH (r = 0·348; P 0·01) and TBARS (r = 0·367; P 0·01). Plasma NEFA decreased overall in both groups (P 0·01). EXP was lower than CTR in concentrations of plasma BOHB at 70 DIM (P 0·05) and plasma insulin at 60 (P 0·001), 80 and 94 (P 0·05) DIM. Plasma TBARS, GSH and GPx increased throughout (P 0·01) in both groups. This was delayed in the EXP group following introduction of LSD; significant differences between groups at 60 (P 0·01), 80 and 95 (P 0·05) DIM for TBARS, and at 70 (P 0·01) and 80 (P 0·05) DIM for GPx. Indicators of immune response and plasma bicarbonates did not differ between groups. Blood pH was significantly lower in the EXP group at 80 and 94 DIM (P 0·001). Blood pCO2 was significantly lower at 80 and 94 DIM (P 0·05) in the CTR group. While recovering from the negative energy balance, cellular metabolism probably shifted towards oxidative phosphorylation, with a consequent oxidative stress increase. LSD delayed this recovery in the EXP group and thus reduced GSH synthesis. In conclusion, the diet starch content may alter the control of oxidative stress and expose animals to oxidative injuries.