scholarly journals Regulation of rat mammary-gland uptake of orally administered [1-14C]triolein by insulin and prolactin: evidence for bihormonal control of lipoprotein lipase activity

1994 ◽  
Vol 300 (1) ◽  
pp. 257-262 ◽  
Author(s):  
T H M Da Costa ◽  
D H Williamson

The effects of insulin deficiency (streptozotocin-induced) or insulin plus prolactin deficiency on the disposal of orally administered [1-14C]triolein between oxidation to 14CO2, uptake by mammary gland and transfer to suckling pups were studied. Insulin deficiency decreased mammary-gland total weight (by 40%), but caused no change in total tissue DNA. A greater proportion of the [1-14C]triolein was oxidized to 14CO2 (120% increase) in the insulin-deficient rats, and there was a tendency for total transfer of [14C]lipid to mammary gland and suckling pups to be decreased. A parallel decrease in total mammary-tissue lipoprotein lipase activity occurred. Combined hormone deficiency caused more dramatic changes in all parameters measured. Replacement of insulin (24 h) in insulin-deficient rats decreased 14CO2 production, increased the uptake of [14C]lipid into the mammary gland and tended to increase total lipoprotein lipase activity. In contrast, administration of prolactin to insulin-deficient rats had no effect on any of the parameters measured. Replacement of insulin (24 h) in the combined hormone-deficient rats increased uptake of [14C]lipid and lipoprotein lipase approx. 3-fold, whereas prolactin again had no significant effects. Replacement of both hormones increased (6-fold) transfer of [14C]lipid to the pups, but did not increase overall uptake of [14C]lipid (mammary gland, milk clot and pups) above the value for insulin alone. It is concluded that insulin is the primary regulator of triacylglycerol uptake and of lipoprotein lipase activity in the lactating mammary gland of the rat and that the action of prolactin on these processes is indirect. Prolactin, but not insulin, appears to have a direct effect on milk lipid transfer to pups.

1994 ◽  
Vol 301 (2) ◽  
pp. 495-501 ◽  
Author(s):  
M Del Prado ◽  
T H Da Costa ◽  
D H Williamson

The effect of tri-iodothyronine (T3) administration on the utilization of dietary [14C]lipid by the mammary gland and adipose tissue of lactating and litter-removed rats was studied. (1) After an oral load of [1-14C]triolein, the lactating rats treated with T3 (50 micrograms/100 g body wt.) over 24 h showed an increase in 14CO2 production and a decrease in the total [14C]lipid transferred through the mammary gland that was paralleled by a decrease in tissue lipoprotein lipase (LPL) activity. (2) T3 administration decreased plasma prolactin in the lactating rats. Prolactin replacement in T3-treated rats restored LPL activity in the mammary gland, but did not increase the amount of dietary [14C]lipid transferred to the milk. (3) Chronic T3 administration (4 days) to lactating rats did not affect pup growth or the lipogenic rate in the mammary gland. (4) The administration of T3 to litter-removed rats inhibited the increase of LPL activity in white adipose tissue and decreased the accumulation of dietary [14C]lipid. This decrease was accompanied by increased 14CO2 production and [14C]lipid accumulation in skeletal muscle and heart. (5) It is concluded that hyperthyroidism depresses LPL activity in mammary gland and white adipose tissue, but not in muscle. The increased accumulation of [14C]lipid in muscle and increased production of 14CO2 in lactating and in litter-removed rats treated with T3 is in part due to the decreased total LPL in mammary gland and adipose tissue respectively, which are therefore less able to compete with muscle for the available plasma triacylglycerols.


1999 ◽  
Vol 129 (8) ◽  
pp. 1574-1578 ◽  
Author(s):  
Martha Del Prado ◽  
Salvador Villalpando ◽  
Joaquín Gordillo ◽  
Homero Hernández-Montes

1975 ◽  
Vol 228 (5) ◽  
pp. 1542-1544 ◽  
Author(s):  
MM Garrison ◽  
RO Scow

The effect of prolactin on lipoprotein lipase activity of crop sac, omental adipose tissue, and esophagus was studied in adult female pigeons. Prolactin injected for 4 days, 1 mg/day, increased lipoprotein lipase activity from 17 to 177 U/g in crop sac and from 68 to 118 U/g in adipose tissue, but had no effect on the activity in esophagus, 4 U/g. (10 = 1 mumol of chylomicron triglyceride hydrolyzed to free fatty acid and glycerol per hour.? Prolactin increased the weight of crop sac from 1.4 to 7.2 G. The effect of prolactin on lipoprotein lipase activity and weight of crop sac occurred mostly during the 3rd and 4th days of treatment, whereas the effect on the activity of adipose tissue occurred later, during the 4th day of treatment. Crop "milk" collected from pigeons injected with 2 mg of prolactin daily for 4 days contained a small amount of lipoprotein lipase activity, 12 U/g, is smaller than 10% of that found in crop sac. The finding of markedly increased lipoprotein lipase activity in crop sac of prolactin-treated pigeons suggests that blood triglyceride may be used by crop sac for the formation of crop milk lipid.


Nutrition ◽  
2004 ◽  
Vol 20 (9) ◽  
pp. 806-811 ◽  
Author(s):  
Renata Pereira Assumpção ◽  
Flávia Duarte dos Santos ◽  
Priscila de Mattos Machado Andrade ◽  
Giselle Freire Barreto ◽  
Maria das Graças Tavares do Carmo

1994 ◽  
Vol 298 (2) ◽  
pp. 321-327 ◽  
Author(s):  
D R Jensen ◽  
S Gavigan ◽  
V Sawicki ◽  
D L Witsell ◽  
R H Eckel ◽  
...  

We examined the effects of reproductive stage and fasting on lipoprotein lipase (LPL) activity and mRNA in the mouse mammary gland. Heparin-releasable and cell-associated LPL activity rose immediately after birth, followed 1-2 days later by an increase in LPL mRNA. Fasting decreased LPL activity in the mammary gland at all reproductive stages. During lactation, both milk and heparin-releasable LPL were substantially decreased by an overnight fast, whereas cell-associated LPL was less affected and LPL mRNA did not change. These studies indicate that the extracellular, heparin-releasable, fraction of mammary LPL activity responds most rapidly to alterations in physiological state, usually accompanied by smaller changes in cellular enzyme activity. Changes in the level of LPL mRNA were seen only during the transition from pregnancy to lactation, and these tended to follow, rather than precede, changes in enzyme activity. We conclude that in the mammary gland as in adipose tissue, LPL is regulated primarily at the translational and post-translational level.


Diabetes ◽  
1979 ◽  
Vol 28 (10) ◽  
pp. 893-898 ◽  
Author(s):  
Y.-D. I. Chen ◽  
T. R. Risser ◽  
M. Cully ◽  
G. M. Reaven

1993 ◽  
Vol 290 (2) ◽  
pp. 557-561 ◽  
Author(s):  
T H M Da Costa ◽  
D H Williamson

The effects of exogenous insulin or vanadate (an insulin mimetic) on the disposal of dietary [14C]lipid between oxidation to 14CO2, deposition in adipose tissue or uptake by mammary gland and transfer to suckling pups were studied in virgin and lactating rats. After an oral load of [1-14C]triolein, virgin rats treated with a supraphysiological dose of insulin over 24 h showed a decrease (58%) in 14CO2 production and increased accumulation of [14C]lipid in carcass and white adipose tissue. There was a 2.5-fold increase in lipoprotein lipase activity in the latter. Chronic vanadate administration (12 days) had no effect on these parameters. In lactating rats, the stimulation of the deposition of [14C]lipid in adipose tissue by exogenous insulin was about 10% of that in virgin rats. In prolactin-deficient lactating rats there was no stimulation of [14C]lipid deposition in adipose tissue by insulin. However, both insulin and vanadate treatment increased the accumulation of [14C]lipid in mammary gland to the values seen in the mammary glands plus pups of normal lactating rats. Lipoprotein lipase activity in the gland was also restored to normal values. It is concluded that in lactation there is resistance to insulin stimulation of dietary lipid deposition in adipose tissue, and that this is not due to circulating prolactin. In addition, exogenous insulin plays a role in the regulation of lipoprotein lipase and hence of dietary lipid uptake into lactating mammary gland.


1988 ◽  
Vol 252 (1) ◽  
pp. 65-72 ◽  
Author(s):  
R D Evans ◽  
D H Williamson

1. The effect of tumour burden on lipid metabolism was examined in virgin, lactating and litter-removed rats. 2. No differences in food intake or plasma insulin concentrations were observed between control animals and those bearing the Walker-256 carcinoma (3-5% of body wt.) in any group studied. 3. In virgin tumour-bearing animals, there was a significant increase in liver mass, blood glucose and lactate, and plasma triacylglycerol; the rate of oxidation of oral [14C]lipid to 14CO2 was diminished, and parametrial white adipose tissue accumulated less [14C]lipid compared with pair-fed controls. 4. These findings were accompanied by increased accumulation of lipid in plasma and decreased white-adipose-tissue lipoprotein lipase activity. 5. In lactating animals, tumour burden had little effect on the accompanying hyperphagia or on pup weight gain; tissue lipogenesis was unaffected, as was tissue [14C]lipid accumulation, plasma [triacylglycerol] and white-adipose-tissue and mammary-gland lipoprotein lipase activity. 6. On removal (24 h) of the litter, the presence of the tumour resulted in decreased rates of lipogenesis in the carcass, liver and white and brown adipose tissue, decreased [14C]lipid accumulation in white adipose tissue, but increased accumulation in plasma and liver, increased plasma [triacylglycerol] and decreased lipoprotein lipase activity in white adipose tissue. 7. The rate of triacylglycerol/fatty acid substrate cycling was significantly decreased in white adipose tissue of virgin and litter-removed rats bearing the tumour, but not in lactating animals. 8. These results demonstrate no functional impairment of lactation, despite the presence of tumour, and the relative resistance of the lactating mammary gland to the disturbance of lipid metabolism that occurs in white adipose tissue of non-lactating rats with tumour burden.


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