scholarly journals Comparison of glucose metabolism in the lactating mammary gland of the rat in vivo and in vitro. Effects of starvation, prolactin or insulin deficiency

1977 ◽  
Vol 164 (1) ◽  
pp. 153-159 ◽  
Author(s):  
Alison M. Robinson ◽  
Dermot H. Williamson
Keyword(s):  
Mammary Gland ◽  
Treated Group ◽  
Suitable Model ◽  
Short Term ◽  
Lactating Mammary Gland ◽  
Group 3 ◽  
Lactate And Pyruvate ◽  
In Vitro Effects

1. Measurements of arteriovenous differences across mammary glands of normal and starved lactating rats, and lactating rats made short-term insulin-deficient with streptozotocin or prolactin-deficient with bromocryptine, showed that only in the starved animals was there a significant decrease in glucose uptake. This decrease was accompanied by release of lactate and pyruvate from the gland, in contrast with the uptake of these metabolites by glands of normal lactating rats. 2. There were no marked differences in metabolite concentrations in freeze-clamped glands in the four conditions studied, apart from a decrease in [lactate] and [pyruvate] and an increase in [glucose] in the glands of the streptozotocin-treated group. 3. Acini isolated from the glands of starved, insulin or prolactin-deficient rats had a higher production of lactate and pyruvate from glucose than did glands from normal rats; this is in agreement with the reported decrease in the proportion of active pyruvate dehydrogenase in these situations [Field & Coore (1976) Biochem. J.156, 333–337; Kankel & Reinauer (1976) Diabetologia12, 149–154]. 4. Addition of insulin did not increase the uptake of glucose by acini from normal glands, but it caused a significant increase in the utilization of glucose by acini from glands of starved rats. Insulin did not decrease the accumulation of lactate and pyruvate in any of the experiments. 5. It is concluded that isolated acini represent a suitable model for the study of mammary-gland carbohydrate metabolism in that they reflect metabolism of the gland in vivo.

A distal region, hypersensitive to DNase I, plays a key role in regulating rabbit whey acidic protein gene expression

2001 ◽  
Vol 359 (3) ◽  
pp. 557-565 ◽  
Author(s):  
Benjamin MILLOT ◽  
Marie-Louise FONTAINE ◽  
Dominique THEPOT ◽  
Eve DEVINOY
Keyword(s):  
Mammary Gland ◽  
Sequence Similarity ◽  
Distal Region ◽  
Dnase I ◽  
Whey Acidic Protein ◽  
Acidic Protein ◽  
Upstream Region ◽  
Lactating Mammary Gland

The aim of the present study was to identify the functional domains of the upstream region of the rabbit whey acidic protein (WAP) gene, which has been used with considerable efficacy to target the expression of several foreign genes to the mammary gland. We have shown that this region exhibits three sites hypersensitive to DNase I digestion in the lactating mammary gland, and that all three sites harbour elements which can bind to Stat5 in vitro in bandshift assays. However, not all hypersensitive regions are detected at all stages from pregnancy to weaning, and the level of activated Stat5 detected in the rabbit mammary gland is low except during lactation. We have studied the role of the distal site, which is only detected during lactation, in further detail. It is located within a 849bp region that is required to induce a strong expression of the chloramphenicol acetyltransferase reporter gene in transfected mammary cells. Taken together, these results suggest that this region, centred around a Stat5-binding site and surrounded by a variable chromatin structure during the pregnancy–lactation cycle, may play a key role in regulating the expression of this gene in vivo. Furthermore, this distal region exhibits sequence similarity with a region located around 3kb upstream of the mouse WAP gene. The existence of such a distal region in the mouse WAP gene may explain the differences in expression between 4.1 and 2.1kb mouse WAP constructs.

Short-term effect of aldosterone on NEM-sensitive ATPase in rat collecting tubule

1989 ◽  
Vol 257 (2) ◽  
pp. F177-F181 ◽  
Author(s):  
C. Khadouri ◽  
S. Marsy ◽  
C. Barlet-Bas ◽  
A. Doucet
Keyword(s):  
Atpase Activity ◽  
Affinity Constant ◽  
Short Term ◽  
Collecting Tubule ◽  
Lag Period ◽  
In Vitro Effects ◽  
Collecting Tubules

Because previous studies indicated that in the collecting tubule, N-ethylmaleimide (NEM)-sensitive ATPase, the biochemical equivalent of the proton pump, is controlled by mineralocorticoids in the long term, the present study was designed to investigate whether such control also exists in the short term. Therefore we investigated the in vivo and in vitro effects of aldosterone on the enzyme activity in cortical and outer medullary collecting tubules (CCT and MCT, respectively) from adrenalectomized rats. Administration of aldosterone (10 micrograms/kg body wt) markedly stimulated NEM-sensitive ATPase activity in the CCT and MCT within 3 h. Similarly, incubating CCT or MCT for 3 h in the presence of 10(-8) M aldosterone enhanced NEM-sensitive ATPase activity up to values similar to those previously measured in the corresponding nephron segments of normal rats. In vitro stimulation of NEM-sensitive ATPase was dose dependent in regard to aldosterone (apparent affinity constant approximately 10(-9) M), appeared after a 30-min lag period, and reached its maximum after 2-2.5 h. Finally, actinomycin D and cycloheximide totally abolished the in vitro action of aldosterone, demonstrating the involvement of protein synthesis in this process.

In-vivo and in-vitro effects of short-term statin pretreatment on coronary relaxation and injury

2012 ◽  
Vol 60 (S 01) ◽  
Author(s):  
AC Deppe ◽  
OJ Liakopoulos ◽  
EW Kuhn ◽  
I Slottosch ◽  
J Geissen ◽  
...  
Keyword(s):  
Short Term ◽  
In Vitro Effects ◽  
Coronary Relaxation

scholarly journals Regulation of lactating-rat mammary-gland lipogenesis by insulin and glucagon in vivo. The role and site of action of insulin in the transition to the starved state

1984 ◽  
Vol 223 (2) ◽  
pp. 345-351 ◽  
Author(s):  
R G Jones ◽  
V Ilic ◽  
D H Williamson
Keyword(s):  
Mammary Gland ◽  
Adaptive Mechanism ◽  
Intracellular Metabolite ◽  
Short Term ◽  
Regulatory Enzymes ◽  
Metabolite Concentrations ◽  
Site Of Action ◽  
Lactating Mammary Gland ◽  
Rat Mammary Gland

Starvation for 6h and 24h caused an 80% and 95% decrease in the rate of mammary-gland lipogenesis respectively in conscious lactating rats. 2. Plasma insulin concentrations decreased and circulating ketone-body concentrations increased with the length of starvation. 3. The inhibition of lipogenesis after 24h starvation was accompanied by increased concentrations of glucose, glucose 6-phosphate and citrate in the mammary gland. Qualitatively similar changes were observed after 6h starvation. 4. Infusion of insulin at physiological concentrations caused a 100% increase in the rate of lipogenesis in fed animals and partially reversed the inhibition of lipogenesis caused by starvation. 5. Infusion of insulin tended to reverse the changes seen in intracellular metabolite concentrations. 4. Infusion of glucagon into fed rats caused no change in the rates of lipogenesis in mammary gland, liver or white adipose tissue. 7. It is concluded that (a) insulin acts physiologically to regulate lipogenesis in the mammary gland, (b) hexokinase and phosphofructokinase are important regulatory enzymes in the short-term control of lipogenesis in the mammary gland, which are under the influence of insulin, and (c) the unresponsiveness of mammary-gland lipogenesis in vivo to infusions of glucagon is consistent with an adaptive mechanism which diverts substrate towards the lactating mammary gland and away from other tissues.

scholarly journals The regulation of lipogenesis in vivo in the lactating mammary gland of the rat during the starved-refed transition. Studies wtih acarbose, a glucosidase inhibitor

1987 ◽  
Vol 242 (1) ◽  
pp. 235-243 ◽  
Author(s):  
S W Mercer ◽  
D H Williamson
Keyword(s):  
Mammary Gland ◽  
Time Course ◽  
Chow Diet ◽  
Glucosidase Inhibitor ◽  
Lactating Mammary Gland ◽  
Phosphofructokinase Activity ◽  
Time Course Study ◽  
Fructose 1,6 Bisphosphate

Depression of carbohydrate digestion by oral administration of acarbose, a glucosidase inhibitor, led to a 75% inhibition of the re-activation of lipogenesis in vivo in the mammary gland of 18 h-starved lactating rats refed with 5 g of chow diet. Rates of [1-14C]glucose incorporation in vitro into lipid and CO2 in mammary-gland acini isolated from refed animals were elevated compared with acini from starved rats, but acarbose treatment completely prevented this stimulation. Gastric intubation of glucose led to a large stimulation of lipogenesis in the mammary gland of starved lactating rats, similar to that induced by refeeding with chow diet; this was dependent on the amount of glucose given and the time elapsed between glucose administration and injection of 3H2O for the measurement of lipogenesis. The switch-on of lipogenesis in the mammary gland of starved lactating rats, by refeeding or by intubation of glucose, was associated with a decrease in the ratio of [glucose 6-phosphate]/[fructose 1,6-bisphosphate] in the gland, indicative of an increase in phosphofructokinase activity. A time-course study revealed that the ratio decreased rapidly over the first 30 min of chow refeeding, after which a large surge in lipogenesis was seen. Acarbose, given 25 min after the onset of refeeding, led to a stepwise increase in the ratio, in parallel with the observed decrease in lipogenic activity. It is concluded that the control of lipogenesis in the mammary gland is closely linked to the availability of dietary carbohydrate. An important site of regulation of lipogenesis in the gland appears to be at the level of phosphofructokinase. A possible role of insulin in the regulation of phosphofructokinase activity, and the acute modulation of insulin-sensitivity in the gland during the starved-refed transition, are discussed.

scholarly journals Utlization of d-3-hydroxy[3-14C]butyrate for lipogenesis in vivo in lactating rat mammary gland

1978 ◽  
Vol 176 (2) ◽  
pp. 635-638 ◽  
Author(s):  
A M Robinson ◽  
D H Williamson
Keyword(s):  
Mammary Gland ◽  
Ketone Body ◽  
Nutritional State ◽  
Insulin Deficiency ◽  
Short Term ◽  
Major Site ◽  
Lactating Mammary Gland ◽  
Rat Mammary Gland

Incorporation of D-3-hydroxy[3-14C]butyrate into lipid in vivo suggests that lactating mammary gland is a major site of ketone-body utilization. The incorporation decreases in short-term insulin deficiency (2h) and on starvation (24h), but increases again on refeeding (2h). The activity of cytosolic acetoacetyl-CoA synthetase parallels the changes in nutritional state, but is not affected by short-term insulin deficiency.

Short-term effect of aldosterone on vasopressin-sensitive adenylate cyclase in rat collecting tubule

1993 ◽  
Vol 264 (5) ◽  
pp. F821-F826 ◽  
Author(s):  
G. el Mernissi ◽  
C. Barlet-Bas ◽  
C. Khadouri ◽  
L. Cheval ◽  
S. Marsy ◽  
...  
Keyword(s):  
Adenylate Cyclase ◽  
Affinity Constant ◽  
Short Term ◽  
Collecting Tubule ◽  
Lag Period ◽  
In Vitro Effects ◽  
Collecting Tubules ◽  
Adrenalectomized Rats

Because previous studies indicated that, in the rat collecting tubule, vasopressin (AVP)-sensitive adenylate cyclase (AC) is controlled by mineralocorticoids in the long term, the present study was designed to investigate whether such a control also exists in the short term. Therefore, we investigated the in vivo and in vitro effects of aldosterone on AC activity in cortical and outer medullary collecting tubules (CCD and OMCD, respectively) from adrenalectomized rats. Injection of aldosterone (10 micrograms/kg body wt) to adrenalectomized rats restored within 3 h AVP-sensitive AC activity in the CCD and OMCD up to the levels observed in the corresponding segments of adrenal intact rats. Similarly, incubating CCD or OMCD from adrenalectomized rats for 2.5 h in the presence of 10(-8) M aldosterone enhanced AVP-sensitive AC activity up to values similar to those found in normal rats. In vitro stimulation of AVP-sensitive AC activity was dose dependent with regard to aldosterone [apparent affinity constant (K0.5) approximately 10(-9) M], appeared after a 30-min lag period, and reached its maximum after 2-2.5 h. In addition, it was totally abolished by the antimineralocorticoid spironolactone, whereas the specific glucocorticoid antagonist RU 38486 had no effect. Finally, actinomycin D and cycloheximide totally abolished the in vitro action of aldosterone, demonstrating the involvement of protein synthesis in that process.

scholarly journals Role of pyruvate dehydrogenase and insulin in the regulation of lipogenesis in the lactating mammary gland of the rat during the starved-refed transition

1981 ◽  
Vol 196 (3) ◽  
pp. 831-837 ◽  
Author(s):  
M R Munday ◽  
D H Williamson
Keyword(s):  
Mammary Gland ◽  
Dehydrogenase Activity ◽  
Pyruvate Dehydrogenase ◽  
Regulatory Site ◽  
Acetyl Coa ◽  
Lactating Mammary Gland

Administration of insulin with glucose to starved lactating rats, which activates pyruvate dehydrogenase [M. A. Baxter & H. G. Coore (1978) Biochiem. J. 174, 553-561], restored lipogenesis in mammary gland in vivo to 50% of the value observed in refed (2.5 h) rats. The correlations between pyruvate dehydrogenase activity and the rate of lipogenesis persisted in isolated acini. Activation of pyruvate dehydrogenase in vitro with dichloroacetate increased lipogenesis from [6-14C]glucose in acini from starved and refed rats by 250% and 100% respectively. However, in the presence of dichloroacetate, only 70% of the increased flux through pyruvate dehydrogenase was converted into lipid in acini from starved rats, whereas all of the increase could be accounted for as lipid in acini from refed rats. Addition of insulin plus dichloroacetate was required to obtain maximal rates of lipogenesis in acini from starved rats. Similarly, insulin increased the incorporation of [1-14C]acetate into lipid only in acini from starved rats. Although the activity of pyruvate dehydrogenase plays an important role in the control of mammary-gland lipogenesis, the evidence presented suggests a second regulatory site which is insulin-sensitive and is located after the generation of cytosolic acetyl-CoA.

Anti-obesity role of Aster glehni extract: in vivo and in vitro effects

Planta Medica ◽  
2012 ◽  
Vol 78 (11) ◽  
Author(s):  
HM Lee ◽  
TG Ahn ◽  
CW Kim ◽  
HJ An
Keyword(s):  
In Vitro Effects
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