Glucose Homeostasis during Fetal and Neonatal Period

2016 ◽  
Vol 27 (2) ◽  
pp. 95
Author(s):  
Won Im Cho ◽  
Hye Rim Chung
1985 ◽  
Vol 249 (3) ◽  
pp. E268-E275
Author(s):  
J. P. Pegorier ◽  
C. Simoes-Nunes ◽  
P. H. Duee ◽  
J. Peret ◽  
J. Girard

The fasting hypoglycemia (1.78 +/- 0.29 mmol/l) which develops in 48-h-old pigs is partially reversed (3.85 +/- 0.55 mmol/l) after gastric administration of long-chain triglycerides (LCT). The increase in blood glucose induced by LCT feeding was not secondary to a decreased glucose utilization because glucose disappearance rate increased in LCT-fed piglets but resulted from a twofold increase in glucose appearance. By using the crossover-plot technique, the stimulation of hepatic gluconeogenesis induced by LCT feeding has been localized at 1) the level of pyruvate carboxylase owing to the twofold increase in hepatic acetyl-CoA concentration and 2) the level of glyceraldehyde-3-phosphate dehydrogenase secondary to the increase in reducing equivalents (NADH), which displaces this equilibrium reaction in the direction of gluconeogenesis. As blood lactate, pyruvate, and alanine concentrations increased after LCT feeding, the possible effects of LCT on pyruvate dehydrogenase in peripheral tissues are discussed. These data demonstrate that fatty acids stimulate hepatic gluconeogenesis in 48-h-old fasting piglets and underline the role of fat provision in the regulation of glucose homeostasis during the neonatal period in the pig.


2008 ◽  
Vol 1 (1) ◽  
pp. 65-72 ◽  
Author(s):  
Ricardo Vinícius Ledesma CONTARTEZE ◽  
Clécia Soares de Alencar MOTA ◽  
Camila Aparecida Machado de OLIVEIRA ◽  
José Alexandre Curiacos de Almeida LEME ◽  
Lara Belmudes BOTTCHER ◽  
...  

1988 ◽  
Vol 39 (2) ◽  
pp. 237-244 ◽  
Author(s):  
L BERMAN ◽  
D STRINGER ◽  
S EIN ◽  
B SHANDLING

2020 ◽  
Vol 90 (1-2) ◽  
pp. 113-123
Author(s):  
Ines Schadock ◽  
Barbara G. Freitas ◽  
Irae L. Moreira ◽  
Joao A. Rincon ◽  
Marcio Nunes Correa ◽  
...  

Abstract. β-hydroxy-β-methyl butyrate (HMB) is a bioactive metabolite derived from the amino acid leucine, usually applied for muscle mass increase during physical training, as well as for muscle mass maintenance in debilitating chronic diseases. The hypothesis of the present study is that HMB is a safe supplement for muscle mass gain by strength training. Based on this, the objective was to measure changes in body composition, glucose homeostasis and hepatic metabolism of HMB supplemented mice during strength training. Two of four groups of male mice (n = 6/group) underwent an 8-week training period session (climbing stairs) with or without HMB supplementation (190 mg/kgBW per day). We observed lower body mass gain (4.9 ± 0.43% versus 1.2 ± 0.43, p < 0.001) and increased liver mass (40.9 ± 0.9 mg/gBW versus 44.8 ± 1.3, p < 0.001) in the supplemented trained group compared with the non-supplemented groups. The supplemented trained group had an increase in relative adipose tissue mass (12.4 ± 0.63 mg/gBW versus 16.1 ± 0.88, P < 0.01) compared to the non-supplemented untrained group, and an increase in fasting blood glucose (111 ± 4.58 mg/dL versus 122 ± 3.70, P < 0.05) and insulin resistance (3.79 ± 0.19 % glucose decay/min versus 2.45 ± 0.28, P < 0.05) comparing with non-supplemented trained group. Adaptive heart hypertrophy was observed only in the non-supplemented trained group (4.82 ± 0.05 mg/gBW versus 5.12 ± 0.13, P < 0.05). There was a higher hepatic insulin-like growth factor-1 expression (P = 0.002) in supplemented untrained comparing with non-supplemented untrained group. Gene expression of gluconeogenesis regulatory factors was increased by training and reduced by HMB supplementation. These results confirm that HMB supplementation associated with intensive training protocol drives changes in glucose homeostasis and liver metabolism in mice.


2017 ◽  
Vol 12 (S 01) ◽  
pp. S1-S84
Author(s):  
T Laeger ◽  
C Baumeier ◽  
J Würfel ◽  
A Schürmann
Keyword(s):  

Author(s):  
Hasan Akduman ◽  
Dilek Dilli ◽  
Serdar Ceylaner

AbstractCongenital glucose-galactose malabsorption (CGGM) is an autosomal recessive disorder originating from an abnormal transporter mechanism in the intestines. It was sourced from a mutation in the SLC5A1 gene, which encodes a sodium-dependent glucose transporter. Here we report a 2-day-old girl with CGGM who presented with severe hypernatremic dehydration due to diarrhea beginning in the first hours of life. Mutation analysis revealed a novel homozygous mutation NM_000343.3 c.127G > A (p.Gly43Arg) in the SLC5A1 gene. Since CGGM can cause fatal diarrhea in the early neonatal period, timely diagnosis of the disease seems to be essential.


1972 ◽  
Vol 70 (2) ◽  
pp. 396-408 ◽  
Author(s):  
K.-D. Schulz ◽  
H. Haarmann ◽  
A. Harland

ABSTRACT The present investigation deals with the oestrogen-sensitivity of the female reproductive system during the neonatal period. Newborn female guinea pigs were used as test animals. At different times after a single subcutaneous injection of a physiological dose of 0.1 μg or an unphysiologically high dose of 10 μg 17β-oestradiol/100 g body weight, the RNA- and protein-synthesis was examined in the hypothalamic region, pituitary, cerebral cortex, liver, adrenal gland, ovary and uterus. With a physiological dose an increase in organ weight, protein content, RNA-and protein-synthesis was found only in the uterus. These alterations turned out to be dose-dependent. In addition to the findings in the uterus an inhibition of the aminoacid incorporation rate occurred in the liver following the injection of the high oestradiol dose. As early as 1 hour after the administration of 0.1 μg 17β-oestradiol an almost 100% increase in uterine protein synthesis was detectable. This result demonstrates a high oestrogen-sensitivity of this organ during the neonatal period. All the other organs of the female reproductive system such as the hypothalamus, pituitary and ovary did not show any oestrogen response. Therefore the functional immaturity of the uterus during post partem life is not the result of a deficient hormone sensitivity but is correlated with the absence of a sufficient hormonal stimulus at this time. The investigation on the effects of actinomycin resulted in different reactions in the uterus and liver. In contrast to the liver a paradoxical actinomycin effect was found in the uterus after treatment with actinomycin alone. This effect is characterized by a small inhibition of RNA-synthesis and a 50% increase in protein synthesis. The treatment of the newborn test animals with actinomycin and 17β-oestradiol together abolished the oestrogen-induced stimulation of the uterine RNA-and protein-synthesis. Consequently, the effect of oestrogens during the neonatal period is also connected with the formation of new proteins via an increased DNA-directed RNA-synthesis.


2018 ◽  
Vol 239 (3) ◽  
pp. 313-324 ◽  
Author(s):  
Lewin Small ◽  
Henry Gong ◽  
Christian Yassmin ◽  
Gregory J Cooney ◽  
Amanda E Brandon

One major factor affecting physiology often overlooked when comparing data from animal models and humans is the effect of ambient temperature. The majority of rodent housing is maintained at ~22°C, the thermoneutral temperature for lightly clothed humans. However, mice have a much higher thermoneutral temperature of ~30°C, consequently data collected at 22°C in mice could be influenced by animals being exposed to a chronic cold stress. The aim of this study was to investigate the effect of housing temperature on glucose homeostasis and energy metabolism of mice fed normal chow or a high-fat, obesogenic diet (HFD). Male C57BL/6J(Arc) mice were housed at standard temperature (22°C) or at thermoneutrality (29°C) and fed either chow or a 60% HFD for 13 weeks. The HFD increased fat mass and produced glucose intolerance as expected but this was not exacerbated in mice housed at thermoneutrality. Changing the ambient temperature, however, did alter energy expenditure, food intake, lipid content and glucose metabolism in skeletal muscle, liver and brown adipose tissue. Collectively, these findings demonstrate that mice regulate energy balance at different housing temperatures to maintain whole-body glucose tolerance and adiposity irrespective of the diet. Despite this, metabolic differences in individual tissues were apparent. In conclusion, dietary intervention in mice has a greater impact on adiposity and glucose metabolism than housing temperature although temperature is still a significant factor in regulating metabolic parameters in individual tissues.


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