Appearance of circulating and tissue 14C-lipids after oral 14C-tripalmitate administration in the late pregnant rat

Argilés, Josep Μ.; Herrera, Emílio

doi:10.1016/0026-0495(89)90247-3

Cited by 28 publications

(19 citation statements)

References 23 publications

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“…First of all, the uptake of dietary lipids and the subsequent formation of chylomicrons is a time-consuming process compared with glucose uptake. Based on the literature, we have estimated the contribution of TGs packed in chylomicrons to total plasma TGs to be negligible within the first 80 min after consumption of chow (1,2,4). With gel electrophoresis we confirmed that after 80 min only a minor fraction of lipids is packed in chylomicrons, whereas the effects of the denervation were already apparent after 40 min.…”

Section: Discussionsupporting

confidence: 53%

The autonomic nervous system regulates postprandial hepatic lipid metabolism

Bruinstroop

Fleur

Ackermans

et al. 2013

American Journal of Physiology-Endocrinology and Metabolism

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Bruinstroop E, la Fleur SE, Ackermans MT, Foppen E, Wortel J, Kooijman S, Berbée JF, Rensen PC, Fliers E, Kalsbeek A. The autonomic nervous system regulates postprandial hepatic lipid metabolism. Am J Physiol Endocrinol Metab 304: E1089 -E1096, 2013. First published March 26, 2013; doi:10.1152/ajpendo.00614.2012The liver is a key organ in controlling glucose and lipid metabolism during feeding and fasting. In addition to hormones and nutrients, inputs from the autonomic nervous system are also involved in fine-tuning hepatic metabolic regulation. Previously, we have shown in rats that during fasting an intact sympathetic innervation of the liver is essential to maintain the secretion of triglycerides by the liver. In the current study, we hypothesized that in the postprandial condition the parasympathetic input to the liver inhibits hepatic VLDL-TG secretion. To test our hypothesis, we determined the effect of selective surgical hepatic denervations on triglyceride metabolism after a meal in male Wistar rats. We report that postprandial plasma triglyceride concentrations were significantly elevated in parasympathetically denervated rats compared with control rats (P ϭ 0.008), and VLDL-TG production tended to be increased (P ϭ 0.066). Sympathetically denervated rats also showed a small rise in postprandial triglyceride concentrations (P ϭ 0.045). On the other hand, in rats fed on a six-meals-a-day schedule for several weeks, a parasympathetic denervation resulted in Ͼ70% higher plasma triglycerides during the day (P ϭ 0.001), whereas a sympathetic denervation had no effect. Our results show that abolishing the parasympathetic input to the liver results in increased plasma triglyceride levels during postprandial conditions. parasympathetic; denervation; liver; triglycerides; feeding THE LIVER IS ESSENTIAL for maintaining metabolic equilibrium in the body by storing and releasing large quantities of energy according to changing demands. In the postprandial state the liver plays a central role in storing energy for later use, whereas in the fasted state the liver increases fuel availability for immediate use. These processes are controlled by circulating hormones, such as insulin, and by the availability of different nutrients. It has long been known that the autonomic nervous input to the liver can also alter hepatic function, especially glucose metabolism (27, 28). Next to being a key player in glucose metabolism, the liver is also important for the regulation of lipid metabolism, as it synthesizes and degrades lipids. Recently, various investigators have revealed a role for the autonomic nervous system in the regulation of hepatic lipid metabolism as well (6,18,32).The autonomic nervous system consists of a sympathetic and a parasympathetic branch. Tracing studies have shown that both branches are anatomically connected to the liver and originate from distinct neuronal populations within the hypothalamus (7,17,35). The two autonomic branches are hypothesized to have opposing or complimentary effects on target org...

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Section: Discussionsupporting

confidence: 53%

The autonomic nervous system regulates postprandial hepatic lipid metabolism

Bruinstroop

Fleur

Ackermans

et al. 2013

American Journal of Physiology-Endocrinology and Metabolism

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“…At this stage of gestation there is even a decrease in adiposetissue lipoprotein lipase [20,[23][24][25] which could indicate a decreased tissue uptake of circulating triglycerides. However, the over production of endogenous triglycerides [21] as well as the enhanced arrival to circulation of dietary lipids [26] cause intense maternal hypertriglyceridemia which could compen sate for the reduced lipoprotein lipase activ ity and allow even an enhanced uptake of circulating triglycerides by adipose tissue [26]. Nevertheless, another change in the maternal adipose-tissue metabolism could contribute to such exaggerated fat deposition occurring between days 18 and 19.…”

Section: Discussionmentioning

confidence: 99%

“…An increased synthesis of triglyc erides has been shown in the perfused preg nant rat liver [21], and triglyceride accumu lation in the liver does not become more manifest because this effect is compensated by an enhanced triglyceride output [21], Present findings also show that mamma ry-gland fat accumulation also contributes to maternal fat storage. This change is specially striking during late gestation and may be related to the enhanced uptake of circulating triglycerides by mammary glands [26] for incorporation into milk lipids which is facil itated by the increase in lipoprotein lipase activity that occurs in these glands of preg nant animals 2-3 days before parturition [24, 30,31],…”

Section: Discussionmentioning

confidence: 99%

Carcass and Tissue Fat Content in the Pregnant Rat

López-Luna¹,

Maier²,

Herrera

1991

Neonatology

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The present study in rats was aimed at determining the specific day of pregnancy on which maternal body fat accumulation starts and which tissues are involved. Most of the body weight increase at day 12 of gestation corresponded to conceptus-free maternal weight which progressively increased until the 19th day of gestation after which maternal weight stabilized and the rate of conceptus weight gain became maximal. Maternal carcass fat content progressively increased until day 18 of gestation, increased very markedly on day 19, stabilized between day 19 and 20 and then decreased on day 21. These changes were the opposite of the course of the specific-gravity values. The fresh weight of lumbar fat-pads and mesenteric adipose tissue reflected the changes in carcass fat content throughout gestation. Periuterine adipose-tissue mass declined on day 12 of gestation to be recuperated later, subcutaneous adipose tissue increased on day 12 to decline progressively thereafter and interscapular brown adipose tissue remained stable until day 20 and increased on day 21. With only a few exceptions, the lipid concentration in all these adipose tissues remained stable throughout gestation. Mammary glands and liver weights increased intensely from day 12 and, whereas the lipid concentration in the former was stable, in the latter it decreased on day 12 and increased on days 18 and 19. These results show that in the rat (a) maternal carcass fat accumulation during gestation is not paralleled by the size of the different fat-storing tissues and (b) mammary-gland fat accumulation also contributes to maternal fat storage.

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“…A greater flow of dietary lipids into cir culation may also contribute to maternal hy pertriglyceridemia. Gastrointestinal transit is reduced at late gestation [31,32] whereas lipidic gut absorption, which is not modified [33,34], augments transmission of triglycer ides from dietary fat [34] during the food intake increase typical in gestation [14,35]. Decreased triglyceride removal cannot be ruled out as an additional factor contribut ing to maternal hypertriglyceridemia.…”

Section: Hydrolysis O F Triglyceridesmentioning

confidence: 99%

Lipid Metabolism in Pregnancy

Herrera

Gómez-Coronado

Lasunción³

1987

Neonatology

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On the basis of bibliographic references and new own data, major adaptations of lipid metabolism occurring at late gestation are reviewed. Maternal hypertriglyceridemia at late gestation results from the juxtaposition of several factors: (1) enhanced adipose tissue lipolysis facilitating the availability to the liver of substrates for triglyceride synthesis and contributing to augmented flux of very low density lipoproteins (VLDL) into the circulation; (2) maternal hyperphagia and unmodified gut lipid absorption increasing chylomicron formation from dietary lipid; (3) reduced lipoprotein lipase (LPL) activity in extrahepatic tissues (especially adipose tissue) which does not allow a triglyceride removal proportional to their enhanced production. It is proposed that these changes are also responsible for the altered composition of VLDL in late pregnancy. In conditions of food deprivation the use of glycerol released from adipose tissue as preferential gluconeogenic substrate, and the enhanced maternal ketogenesis warrants the availability of fuels for the fetus. Just prior to parturition the increase in mammary gland LPL activity is responsible for the reduction in circulating triglycerides and prepares the mother for lactation.

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Appearance of circulating and tissue 14C-lipids after oral 14C-tripalmitate administration in the late pregnant rat

Cited by 28 publications

References 23 publications

The autonomic nervous system regulates postprandial hepatic lipid metabolism

The autonomic nervous system regulates postprandial hepatic lipid metabolism

Carcass and Tissue Fat Content in the Pregnant Rat

Lipid Metabolism in Pregnancy

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