Effects of ewe size and nutrition during pregnancy on glucose metabolism, fat metabolism and adrenal function of postpubertal female twin offspring

2010 ◽  
Vol 50 (9) ◽  
pp. 869 ◽  
Author(s):  
D. S. van der Linden ◽  
P. R. Kenyon ◽  
H. T. Blair ◽  
N. Lopez-Villalobos ◽  
C. M. C. Jenkinson ◽  
...  

Little is known about the long-term metabolic effects of maternal constraint on the offspring and whether a possible interaction of dam size and nutrition during gestation exists, affecting postnatal metabolic functions in the offspring. Four hundred and fifty heavy (H) (60.8 ± 0.18 kg) and 450 light (L) (42.5 ± 0.17 kg) Romney dams were allocated to ad libitum (A) or maintenance (M) nutritional regimens under New Zealand pastoral grazing conditions, from Day 21 to 140 after insemination. One week before lambing, all dams and offspring were managed as one group and provided with ad libitum feeding. At 16 months of age, female twin-born offspring (n = 12 per size by nutrition group) were catheterised and given intravenous insulin (0.15 IU/kg) (ITT), glucose (0.17 g/kg) (GTT) and epinephrine (1 μg/kg) (ETT) challenges to assess their glucose and fat metabolism and adrenal function. No effects of dam size or interactions between dam size and dam nutrition were found on glucose or fat metabolism or adrenal function. In response to the ETT, M-dam offspring showed greater (P < 0.05) peak glucose concentrations, increased (P < 0.05) glucose area under the curve and tended (P < 0.10) to have increased maximum change in glucose and non-esterified free fatty acid concentrations compared with A-ewes. No effects of dam nutrition were found on glucose tolerance, insulin resistance or adrenal function in response to GTT and ITT. In conclusion, dam size had no effect on glucose metabolism, adrenal function or fat metabolism in 16-month-old female twin offspring. Dam nutrition during pregnancy from Day 21 to 140 had no major effect on glucose metabolism, adrenal function or lipolysis; however, it did potentially affect gluconeogenesis and/or glycogenolysis, as increased glucose concentrations in ewes born to M-fed dams were observed in response to ETT. These results indicate that M-ewes could have an advantage over A-ewes in physiological stressful situations in life (e.g. pregnancy, lactation) as their liver may be able to supply more glucose to support their growing conceptus and milk production to increase the chances of survival of their offspring.

2015 ◽  
Vol 12 (8) ◽  
pp. 1133-1138 ◽  
Author(s):  
Meredith C. Peddie ◽  
Claire Cameron ◽  
Nancy Rehrer ◽  
Tracy Perry

Background:Interrupting sedentary time induces improvements in glucose metabolism; however, it is unclear how much activity is required to reduce the negative effects of prolonged sitting.Methods:Sixty-six participants sat continuously for 9 hours except for required bathroom breaks. Participants were fed meal replacement beverages at 60, 240 and 420 min. Blood samples were obtained hourly for 9 hours, with additional samples collected 30 and 45 min after each feeding. Responses were calculated as incremental area under the curve (iAUC) for plasma glucose, insulin and triglyceride. Participants wore a triaxial accelerometer and a heart rate monitor. Energy expenditure was estimated using indirect calorimetry.Results:After controlling for age, sex and BMI, every 100 count increase in accelerometer derived total movement was associated with a 0.06 mmol·L-1·9 hours decrease in glucose iAUC (95% CI 0.004–0.1; P = .035), but not associated with changes in insulin or triglyceride iAUC. Every 1 bpm increase in mean heart rate was associated with a 0.76 mmol·L-1·9 hours increase in triglyceride iAUC (95% CI 0.13–1.38).Conclusion:Accelerometer measured movement during periods of prolonged sitting can result in minor improvements in postprandial glucose metabolism, but not lipid metabolism.


2008 ◽  
Vol 100 (5) ◽  
pp. 947-952 ◽  
Author(s):  
Michael M. Swarbrick ◽  
Kimber L. Stanhope ◽  
Sharon S. Elliott ◽  
James L. Graham ◽  
Ronald M. Krauss ◽  
...  

Fructose consumption in the USA has increased over the past three decades. During this time, obesity, insulin resistance and the metabolic syndrome have also increased in prevalence. While diets high in fructose have been shown to promote insulin resistance and increase TAG concentrations in animals, there are insufficient data available regarding the long-term metabolic effects of fructose consumption in humans. The objective of the present study was to investigate the metabolic effects of 10-week consumption of fructose-sweetened beverages in human subjects under energy-balanced conditions in a controlled research setting. Following a 4-week weight-maintaining complex carbohydrate diet, seven overweight or obese (BMI 26·8–33·3 kg/m2) postmenopausal women were fed an isoenergetic intervention diet, which included a fructose-sweetened beverage with each meal, for 10 weeks. The intervention diet provided 15 % of energy from protein, 30 % from fat and 55 % from carbohydrate (30 % complex carbohydrate, 25 % fructose). Fasting and postprandial glucose, insulin, TAG and apoB concentrations were measured. Fructose consumption increased fasting glucose concentrations and decreased meal-associated glucose and insulin responses (P = 0·0002,P = 0·007 andP = 0·013, respectively). Moreover, after 10 weeks of fructose consumption, 14 h postprandial TAG profiles were significantly increased, with the area under the curve at 10 weeks being 141 % higher than at baseline (P = 0·04). Fructose also increased fasting apoB concentrations by 19 % (P = 0·043v.baseline). In summary, consumption of fructose-sweetened beverages increased postprandial TAG and fasting apoB concentrations, and the present results suggest that long-term consumption of diets high in fructose could lead to an increased risk of CVD.


2021 ◽  
Vol 2 (Supplement_1) ◽  
pp. A23-A24
Author(s):  
S Centofanti ◽  
L Heilbronn ◽  
G Wittert ◽  
A Coates ◽  
J Dorrian ◽  
...  

Abstract Nightwork disrupts circadian rhythms and impairs glucose metabolism, increasing the risk for type 2 diabetes. We investigated eliminating or reducing the amount of food consumed during simulated nightwork as a countermeasure to reduce the impact of circadian disruption on glucose metabolism. N=52 healthy, non-shiftworking participants (24.4±4.9 years; 26 Females; BMI 23.8±2.5kg/m2) underwent a 7-day laboratory protocol with an 8h TIB baseline sleep, followed by 4 simulated nightshifts with 7h TIB daytime sleep and an 8h TIB recovery sleep in groups of 4 participants. Each group was randomly assigned to a meal-at-midnight (n=17, 30% energy requirements), snack-at-midnight (n=16, 10% energy requirements) or no-eating-at-midnight (n=19) condition. Total 24h energy and macronutrient intake were constant across conditions. Standard oral glucose tolerance tests (OGTT) were conducted on day2 (baseline), and day7 (recovery). Plasma was sampled at -15, 0, 15, 30, 60, 90, 120, 150 mins, assayed for glucose and insulin. Area under the curve (AUC) was the calculated. Mixed model analyses of glucose AUC found a condition-by-day interaction (p&lt;0.001). Glucose responses to OGTT did not change with nightwork in the no-eating-at-midnight condition (p=0.219) but worsened in the meal-at-midnight (p&lt;0.001) and snack-at-midnight (p=0.022) conditions. Insulin AUC was different by condition (p=0.047). Insulin was highest after nightwork in the no-eating-at-midnight compared to meal-at-midnight (p=0.014) but not snack-at-midnight (p=0.345). Glucose tolerance was impaired by eating-at-midnight, associated with a lower than expected insulin response. Further work is required to determine the effect of meal or snack composition as a strategy to mitigate adverse metabolic effects of nightwork.


2020 ◽  
Author(s):  
P Köhli ◽  
J Appelt ◽  
D Jahn ◽  
E Otto ◽  
A Baranowsky ◽  
...  

1971 ◽  
Vol 68 (1_Supplb) ◽  
pp. S198
Author(s):  
Harald Frey ◽  
D. Falch ◽  
K. Forfang ◽  
N. Norman ◽  
D. Fremstad
Keyword(s):  

1969 ◽  
Vol 61 (1_Suppl) ◽  
pp. S113
Author(s):  
J. R. Hodges ◽  
Janet Sadow
Keyword(s):  

Cancers ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 396
Author(s):  
Timon A. Bloedjes ◽  
Guus de Wilde ◽  
Jeroen E. J. Guikema

Oncogene activation and malignant transformation exerts energetic, biosynthetic and redox demands on cancer cells due to increased proliferation, cell growth and tumor microenvironment adaptation. As such, altered metabolism is a hallmark of cancer, which is characterized by the reprogramming of multiple metabolic pathways. Multiple myeloma (MM) is a genetically heterogeneous disease that arises from terminally differentiated B cells. MM is characterized by reciprocal chromosomal translocations that often involve the immunoglobulin loci and a restricted set of partner loci, and complex chromosomal rearrangements that are associated with disease progression. Recurrent chromosomal aberrations in MM result in the aberrant expression of MYC, cyclin D1, FGFR3/MMSET and MAF/MAFB. In recent years, the intricate mechanisms that drive cancer cell metabolism and the many metabolic functions of the aforementioned MM-associated oncogenes have been investigated. Here, we discuss the metabolic consequences of recurrent chromosomal translocations in MM and provide a framework for the identification of metabolic changes that characterize MM cells.


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