Pregnancy and pentobarbital anaesthesia modify hepatic synthesis of acylglycerol glycerol and glycogen from gluconeogenic precursors during fasting in rats

Zorzano, António; Herrera, Emílio

doi:10.1042/bj2560487

Cited by 7 publications

(3 citation statements)

References 37 publications

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“…Despite the presence of accelerated fasting, the rates of gluconeogenesis after an overnight fast do not differ between pregnant and nonpregnant dogs (7), and incorporation of labeled alanine or glycerol into plasma glucose or hepatic glycogen is indistinguishable in 24-h-fasted virgin and late-pregnant rats (49). Consistent with this, hepatic PEPCK protein was very similar in the N and P groups.…”

Section: Discussionmentioning

confidence: 99%

Hepatic Glucose Metabolism in Late Pregnancy

et al. 2013

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Net hepatic glucose uptake (NHGU) is an important contributor to postprandial glycemic control. We hypothesized that NHGU is reduced during normal pregnancy and in a pregnant diet-induced model of impaired glucose intolerance/gestational diabetes mellitus (IGT/GDM). Dogs (n = 7 per group) that were nonpregnant (N), normal pregnant (P), or pregnant with IGT/GDM (pregnant dogs fed a high-fat and -fructose diet [P-HFF]) underwent a hyperinsulinemic-hyperglycemic clamp with intraportal glucose infusion. Clamp period insulin, glucagon, and glucose concentrations and hepatic glucose loads did not differ among groups. The N dogs reached near-maximal NHGU rates within 30 min; mean ± SEM NHGU was 105 ± 9 µmol⋅100 g liver−1⋅min−1. The P and P-HFF dogs reached maximal NHGU in 90–120 min; their NHGU was blunted (68 ± 9 and 16 ± 17 µmol⋅100 g liver−1⋅min−1, respectively). Hepatic glycogen synthesis was reduced 20% in P versus N and 40% in P-HFF versus P dogs. This was associated with a reduction (>70%) in glycogen synthase activity in P-HFF versus P and increased glycogen phosphorylase (GP) activity in both P (1.7-fold greater than N) and P-HFF (1.8-fold greater than P) dogs. Thus, NHGU under conditions mimicking the postprandial state is delayed and suppressed in normal pregnancy, with concomitant reduction in glycogen storage. NHGU is further blunted in IGT/GDM. This likely contributes to postprandial hyperglycemia during pregnancy, with potential adverse outcomes for the fetus and mother.

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Section: Discussionmentioning

confidence: 99%

Hepatic Glucose Metabolism in Late Pregnancy

et al. 2013

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“…Since insulin/glucose interactions seem to play an important role in the overall metabolic adaptations taking place during pregnancy, the present experimental study in rats was addressed to determining the circu lating glucose and insulin levels, the pancreat ic insulin content and the short-time hypogly cemic response to a high dose of insulin as index of insulin responsiveness at different days of gestation. Since anesthesia is known to exaggerate the insulin response to glucose in nonpregnant rats [19] and even to affect the glucose metabolism in a different manner in pregnant and nonpregnant animals [20,21], the animals used for this study were unanes thetized.…”

Section: Introductionmentioning

confidence: 99%

Glucose and Insulin Tolerance Tests in the Rat on Different Days of Gestation

Muñoz

López-Luna²,

Herrera³

1995

Neonatology

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To study insulin/glucose relationship during gestation, rats were studied on days 6, 12, 15, 18, 20 or 21 of pregnancy and the results were compared to values in sex-matched virgin control rats. Blood glucose levels were decreased on days 20 and 21 of gestation whereas plasma insulin levels appeared decreased on days 6 and 12, unchanged on day 15 and enhanced on days 18, 20 and 21 of gestation. Total pancreas insulin content was already augmented on day 6 of gestation and continued to increase with gestational time. With the exception of an increase in the 6-day-pregnant rats 22.5 min after an oral glucose load, blood glucose levels did not differ between 6- or 12-day-pregnant rats and virgin controls although plasma insulin levels reached higher values on these days. However, in the 15-day-pregnant rats, glucose tolerance after the glucose load was enhanced while plasma insulin levels did not differ from those in virgin rats during the first 30 min. In the 18-day-pregnant rat blood glucose was more increased but plasma insulin did not differ after the glucose load when compared to virgin rats, whereas 20- or 21-day-pregnant rats showed a glucose tolerance similar to that of virgin rats but their insulin levels shortly after the glucose load were higher. The hypoglycemic response to a high intravenous dose of insulin was decreased in 12-, 18-, 20- and 21-day-pregnant rats. Therefore, whereas in both the 6-and 12-day-pregnant rats there is an enhanced β-cell response to the glucose insulinotropic effect and insulin responsiveness is reduced in 12-day-pregnant rats, the 15-day pregnant rat is in a transitory stage where both insulin sensitivity and the β-cell response return to nonpregnant values. However, from 18 days of gestation on, there is an intense insulin-resistant condition which is only partially compensated by an enormous accumulation of insulin in the pancreas followed by a faster and larger insulin release after a glucose load.

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“…Glucose turnover, using 3 H-glucose as a tracer, show that a transient increase in hepatic glucose production occurs and peripheral tissue glucose uptake decreases by 30% as compared with conscious rats (133). Pentobarbital anesthesia increases hepatic synthesis of glycogen from the gluconeogenic precursors alanine and pyruvate in rats (134). From these data it is clear that the hyperinsulinaemic, euglycaemic clamp technique should be performed in conscious rats.…”

Section: • Anesthesiamentioning

confidence: 87%

In vivo insulin action and resistance. The hyperinsulinaemic, euglycaemic clamp technique in conscious rats

Koopmans

Radder

1996

Biomedical Reviews

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• After almost 75 years of research and four Nobel prizes awarded for insulin-related investigations, we still do not understand how insulin works. Of course, substantial progress has been made and there are some clues. We review in vivo insulin action from the moment of insulin biosynthesis in the pancreatic fi-cell to insulin action on effector systems in target tissues. The mechanism of insulin action at the whole body, tissue and cellular level is discussed. In addition, factors and conditions influencing insulin action and events leading to insulin resistance are summarized. Finally, the reader is introduced into the principles of the hyperinsulinaemic, euglycaemic clamp technique which is considered the "golden standard" for measurement of insulin action and resistance in vivo. An example is given how to clamp conscious rats in a proper way.

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Pregnancy and pentobarbital anaesthesia modify hepatic synthesis of acylglycerol glycerol and glycogen from gluconeogenic precursors during fasting in rats

Cited by 7 publications

References 37 publications

Hepatic Glucose Metabolism in Late Pregnancy

Hepatic Glucose Metabolism in Late Pregnancy

Glucose and Insulin Tolerance Tests in the Rat on Different Days of Gestation

In vivo insulin action and resistance. The hyperinsulinaemic, euglycaemic clamp technique in conscious rats

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