scholarly journals Evidence for conservation of dietary lipid in the rat during lactation and the immediate period after removal of the litter. Decreased oxidation of oral [1-14C]triolein

1986 ◽  
Vol 239 (1) ◽  
pp. 233-236 ◽  
Author(s):  
C M Oller do Nascimento ◽  
D H Williamson
Keyword(s):  
Adipose Tissue ◽  
Mammary Gland ◽  
Lipoprotein Lipase ◽  
Relative Activity ◽  
Dietary Lipid ◽  
Litter Removal ◽  
Lactating Mammary Gland ◽  
14Co2 Production

Production of 14CO2 from an oral load of [1-14C]triolein was greatly decreased (70%) in lactating rats or immediately after (24-48 h) removal of the litter, compared with virgin rats. This decreased oxidation of dietary lipid was accompanied by accumulation of 14C-labelled lipid in lactating mammary gland or adipose tissue (after litter removal). No difference in 14CO2 production between lactating and virgin rats was observed when [1-14C]octanoate was administered. It is concluded that a major factor in this conservation of dietary triacylglycerol is the relative activity of lipoprotein lipase in the tissues.

scholarly journals Effects of tri-iodothyronine administration on the disposal of oral [1-14C]triolein, lipoprotein lipase activity and lipogenesis in the rat during lactation and on removal of the litter

1994 ◽  
Vol 301 (2) ◽  
pp. 495-501 ◽  
Author(s):  
M Del Prado ◽  
T H Da Costa ◽  
D H Williamson
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Mammary Gland ◽  
Lipoprotein Lipase ◽  
White Adipose Tissue ◽  
Lipase Activity ◽  
Plasma Prolactin ◽  
Lipoprotein Lipase Activity ◽  
14Co2 Production ◽  
Pup Growth

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.

scholarly journals Tissue-specific effects of starvation and refeeding on the disposal of oral [1-14C]triolein in the rat during lactation and on removal of litter

1988 ◽  
Vol 254 (2) ◽  
pp. 539-546 ◽  
Author(s):  
C M Oller do Nascimento ◽  
D H Williamson
Keyword(s):  
Adipose Tissue ◽  
Mammary Gland ◽  
Brown Adipose Tissue ◽  
Lipoprotein Lipase ◽  
White Adipose Tissue ◽  
Lipid Accumulation ◽  
Milk Lipid ◽  
Plasma Insulin Concentration ◽  
Brown Adipose ◽  
14Co2 Production

1. The effects of starvation and refeeding on the disposal of oral [14C]triolein between 14CO2 production and 14C-lipid accumulation in tissues of virgin rats, lactating rats and lactating rats with pups removed were studied. 2. Starvation (24 h) increased 14CO2 production in lactating rats and lactating rats with pups removed to values found in virgin rats. This increase was accompanied by decreases in 14C-lipid accumulation in mammary gland and pups of lactating rats and in white and brown adipose tissue of lactating rats with pups removed. 3. Short-term (2 h) refeeding ad libitum decreased 14CO2 production in lactating rats and lactating rats with pups removed, and restored the 14C-lipid accumulation in mammary glands plus pups and in white and brown adipose tissue respectively 4. Insulin deficiency induced with mannoheptulose inhibited the restoration of 14C-lipid accumulation in white adipose tissue on refeeding of lactating rats with pups removed, but did not prevent the restoration of 14C-lipid accumulation in mammary gland. 5. Changes in the activity of lipoprotein lipase in mammary gland and white adipose tissue paralleled the changes in 14C-lipid accumulation in these tissues. 6. It is concluded that 14C-lipid accumulation in mammary gland may not be affected by changes in plasma insulin concentration and that it is less sensitive to starvation than is lipogenesis or lactose synthesis. This has the advantage that the milk lipid content can still be maintained from hepatic very-low-density lipoprotein for a period after withdrawal of food. The major determinant of the disposal of oral 14C-triolein appears to be the total tissue activity of lipoprotein lipase. When this is high in mammary gland (fed lactating rats) or white adipose tissue (fed lactating rats with pups removed), less triacylglycerol is available for the muscle mass and consequently less is oxidized.

scholarly journals Effects of exogenous insulin or vanadate on disposal of dietary triacylglycerols between mammary gland and adipose tissue in the lactating rat: insulin resistance in white adipose tissue

1993 ◽  
Vol 290 (2) ◽  
pp. 557-561 ◽  
Author(s):  
T H M Da Costa ◽  
D H Williamson
Keyword(s):  
Adipose Tissue ◽  
Mammary Gland ◽  
Lipoprotein Lipase ◽  
White Adipose Tissue ◽  
Lipase Activity ◽  
Dietary Lipid ◽  
Lipid Deposition ◽  
Exogenous Insulin ◽  
Lipoprotein Lipase Activity ◽  
Stimulation Of

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.

scholarly journals A High Dietary Lipid Intake during Pregnancy and Lactation Enhances Mammary Gland Lipid Uptake and Lipoprotein Lipase Activity in Rats

1999 ◽  
Vol 129 (8) ◽  
pp. 1574-1578 ◽  
Author(s):  
Martha Del Prado ◽  
Salvador Villalpando ◽  
Joaquín Gordillo ◽  
Homero Hernández-Montes
Keyword(s):  
Mammary Gland ◽  
Lipoprotein Lipase ◽  
Lipase Activity ◽  
Dietary Lipid ◽  
Lipid Uptake ◽  
Lipoprotein Lipase Activity ◽  
Pregnancy And Lactation

scholarly journals Evidence that use of Triton WR1339 underestimates the triacylglycerol entry rate into the plasma of lactating rats owing to continued accumulation of lipid in the mammary gland

1990 ◽  
Vol 272 (3) ◽  
pp. 835-838 ◽  
Author(s):  
A E Tedstone ◽  
V Ilic ◽  
D H Williamson
Keyword(s):  
Adipose Tissue ◽  
Mammary Gland ◽  
Lipoprotein Lipase ◽  
White Adipose Tissue ◽  
Entry Rate

Measurement of the entry rate of an intragastric load of [14C]triolein into the plasma in the presence of Triton WR1339 gave similar values for virgin and weaned rats, but significantly lower values for lactating rats. This decreased entry rate (65%) in lactating compared with virgin rats was due to a failure of Triton WR1339 to inhibit the accumulation of [14C]lipid in the mammary gland. This is further evidence that mammary-gland lipoprotein lipase behaves differently from that in white adipose tissue or muscle.

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
Keyword(s):  
Mammary Gland ◽  
Lipoprotein Lipase ◽  
Lipase Activity ◽  
Hormone Deficiency ◽  
Mammary Tissue ◽  
Milk Lipid ◽  
Lipid Transfer ◽  
Insulin Deficiency ◽  
Lipoprotein Lipase Activity ◽  
Lactating Mammary Gland

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.

scholarly journals Lipoprotein lipase and the disposition of dietary fatty acids

1998 ◽  
Vol 80 (6) ◽  
pp. 495-502 ◽  
Author(s):  
Barbara A. Fielding ◽  
Keith N. Frayn
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Mammary Gland ◽  
Fatty Acid ◽  
Lipoprotein Lipase ◽  
White Adipose Tissue ◽  
Dietary Fatty Acids ◽  
The Body ◽  
Acid Uptake ◽  
Peripheral Tissues

Lipoprotein lipase (EC 3.1.1.34; LPL) is a key enzyme regulating the disposal of lipid fuels in the body. It is expressed in a number of peripheral tissues including adipose tissue, skeletal and cardiac muscle and mammary gland. Its role is to hydrolyse triacylglycerol (TG) circulating in the TG-rich lipoprotein particles in order to deliver fatty acids to the tissue. It appears to act preferentially on chylomicron-TG, and therefore may play a particularly important role in regulating the disposition of dietary fatty acids. LPL activity is regulated according to nutritional state in a tissue-specific manner according to the needs of the tissue for fatty acids. For instance, it is highly active in lactating mammary gland; in white adipose tissue it is activated in the fed state and suppressed during fasting, whereas the reverse is true in muscle. Such observations have led to the view of LPL as a metabolic gatekeeper, especially for dietary fatty acids. However, closer inspection of its action in white adipose tissue reveals that this picture is only partially true. Normal fat deposition in adipose tissue can occur in the complete absence of LPL, and conversely, if LPL activity is increased by pharmacological means, increased fat storage does not necessarily follow. LPL appears to act as one member of a series of metabolic steps which are regulated in a highly coordinated manner. In white adipose tissue, it is clear that there is a major locus of control of fatty acid disposition downstream from LPL. This involves regulation of the pathway of fatty acid uptake and esterification, and appears to be regulated by a number of factors including insulin, acylation-stimulating protein and possibly leptin.

scholarly journals Polymyxin B diminishes blood flow to brown adipose tissue and lactating mammary gland in the rat. Possible mechanism of its action to decrease the stimulation of lipogenesis on refeeding

1989 ◽  
Vol 261 (2) ◽  
pp. 445-450 ◽  
Author(s):  
A E Tedstone ◽  
B Tedoldi ◽  
V Ilic ◽  
D H Williamson
Keyword(s):  
Blood Flow ◽  
Adipose Tissue ◽  
Mammary Gland ◽  
Brown Adipose Tissue ◽  
Glucose Utilization ◽  
Polymyxin B ◽  
Tissue Slices ◽  
Brown Adipose ◽  
Lactating Mammary Gland

Polymyxin B, a cyclic decapeptide antibiotic, increased blood glucose and lactate, and inhibited the stimulation of lipogenesis in interscapular brown adipose tissue and lactating mammary gland of starved-refed virgin and lactating rats respectively. Lipogenesis was not inhibited in white adipose tissue or liver. The antibiotic increased the haematocrit. The relative blood flow to brown adipose tissue and lactating mammary gland was decreased by polymyxin B, and this was accompanied by a decrease in tissue ATP content. In vitro polymyxin B did not affect glucose utilization or conversion into lipid, nor the stimulation by insulin of these processes in brown-adipose-tissue slices. Treatment of rats in vivo with polymyxin B resulted in decreased utilization of glucose in vitro in brown-adipose-tissue slices. Similarly, acini from mammary glands of polymyxin B-treated lactating rats had decreased rates of conversion of [1-14C]glucose to lipid. It is concluded that the effects of polymyxin B may be brought about by decreases in tissue blood flow. The possibility that these effects are secondary to inhibition of glucose utilization cannot be ruled out.

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