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

Muñoz, Carmen; López-Luna, Pilar; Herrera, Emílio

doi:10.1159/000244248

Cited by 32 publications

(33 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Our findings might agree with several studies reporting that ovarian steroids affect -cell function and glucose homeostasis by increasing insulin production through the induction of -cell hypertrophy (YkiJarvinen 1984, Magnaterra et al 1997, Zhu et al 1998, Nieuwenhuizen et al 1999 and, furthermore, with those observing that chronic progesterone therapy has no effect on either basal glucose or insulin levels compared with control rats (Nelson et al 1994). We have previously demonstrated (González et al 1997(González et al , 1998) that the fasting serum insulin levels decreased between days 5 and 10 and increased between days 10 and 15 of pregnancy, findings in line with other studies (Bliss et al 1990, Parsons et al 1992, Muñoz et al 1995. However, in this work, the fasting serum insulin significantly decreased between days 11 and 16 of treatment in the EP group.…”

Section: Discussionsupporting

confidence: 89%

Role of 17beta-estradiol and/or progesterone on insulin sensitivity in the rat: implications during pregnancy

González¹,

Alonso²,

Álvarez³

et al. 2000

Journal of Endocrinology

View full text Add to dashboard Cite

The mechanism for the development of insulin resistance in normal pregnancy is complex and is associated with serum levels of both progesterone and 17 -estradiol. However, it remains unclear whether estrogens alone or progestins alone can cause insulin resistance, or whether it is a combination of both which produces this effect. We attempted to determine the role played by progesterone and/or 17 -estradiol on the phenomena of sensitivity to insulin action that take place during pregnancy in the rat. Ovariectomized rats were treated with different doses of progesterone and/or 17 -estradiol in order to simulate the plasma levels in normal pregnant rats. A euglycemic/ hyperinsulinemic clamp was used to measure insulin sensitivity. At days 6 and 11, vehicle (V)-and progesterone (P)-treated groups were more insulin resistant than 17 -estradiol (E)-and 17 -estradiol+progesterone (EP)-treated groups. Nevertheless, at day 16, the V, EP and E groups were more resistant to insulin action than the P group. On the other hand, the V, EP and E groups were more insulin resistant at day 16 than at day 6, whereas the P group was more insulin resistant at day 6 than at day 16. Our results seem to suggest that the absence of female steroid hormones gives rise to a decreased insulin sensitivity. The rise in insulin sensitivity during early pregnancy, when the plasma concentrations of 17 -estradiol and progesterone are low, could be due to 17 -estradiol. However, during late pregnancy when the plasma concentrations of 17 -estradiol and progesterone are high, the role of 17 -estradiol could be to antagonize the effect of progesterone, diminishing insulin sensitivity.

show abstract

Section: Discussionsupporting

confidence: 89%

Role of 17beta-estradiol and/or progesterone on insulin sensitivity in the rat: implications during pregnancy

González¹,

Alonso²,

Álvarez³

et al. 2000

Journal of Endocrinology

View full text Add to dashboard Cite

show abstract

“…Hyperinsulinemia is a common finding and occurs even before the resistance to insulin occurs in pregnancy (11). There is a correlation between insulin sensitivity and fat accumulation in maternal tissues, since women with decreased insulin sensitivity before pregnancy have difficulty increasing fat mass at the beginning of pregnancy (36).…”

Section: Discussionmentioning

confidence: 99%

“…In the initial stage of pregnancy, fatty acid synthesis from glucose is increased and the lipogenic pathway predominates, whereas in the final stage the lipolytic pathway is more active (10). The net anabolic condition present in the first phase of pregnancy seems to be driven by insulin, the most efficient anabolic hormone, and its pancreatic concentration and secretion are both enhanced from early pregnancy (11,12).…”

Section: Introductionmentioning

confidence: 99%

Correlation of serum leptin and insulin levels of pregnant protein-restricted rats with predictive obesity variables

Macedo

Ferreira

Menegaz

et al. 2008

Braz J Med Biol Res

View full text Add to dashboard Cite

During pregnancy and protein restriction, changes in serum insulin and leptin levels, food intake and several metabolic parameters normally result in enhanced adiposity. We evaluated serum leptin and insulin levels and their correlations with some predictive obesity variables in Wistar rats (90 days), up to the 14th day of pregnancy: control non-pregnant (N = 5) and pregnant (N = 7) groups (control diet: 17% protein), and low-protein non-pregnant (N = 5) and pregnant (N = 6) groups (low-protein diet: 6%). Independent of the protein content of the diet, pregnancy increased total (F 1,19 = 22.28, P < 0.001) and relative (F 1,19 = 5.57, P < 0.03) food intake, the variation of weight (F 1,19 = 49.79, P < 0.000) and final body weight (F 1,19 = 19.52, P < 0.001), but glycemia (F 1,19 = 9.02, P = 0.01) and the relative weight of gonadal adipose tissue (F 1,19 = 17.11, P < 0.001) were decreased. Pregnancy (F 1,19 = 18.13, P < 0.001) and low-protein diet (F 1,19 = 20.35, P < 0.001) increased the absolute weight of brown adipose tissue. However, the relative weight of this tissue was increased only by protein restriction (F 1,19 = 15.20, P < 0.001) and the relative lipid in carcass was decreased in low-protein groups (F 1,19 = 4.34, P = 0.05). Serum insulin and leptin levels were similar among groups and did not correlate with food intake. However, there was a positive relationship between serum insulin levels and carcass fat depots in low-protein groups (r = 0.37, P < 0.05), while in pregnancy serum leptin correlated with weight of gonadal (r = 0.39, P < 0.02) and retroperitoneal (r = 0.41, P < 0.01) adipose tissues. Unexpectedly, protein restriction during 14 days of pregnancy did not alter the serum profile of adiposity signals and their effects on food intake and adiposity, probably due to the short term of exposure to low-protein diet.

show abstract

“…We also wanted to determine whether the decrease in plasma concentration of TG and FFA secondary to the administration of acipimox had any effect either in the OGTT or in the IVIT in 20-day pregnant rats, at the time of increased insulin resistance [15]. As can be seen in Figure 2, after the administration of oral glucose, no differences were observed in plasma glucose concentration between control and acipimox groups, in either pregnant or virgin rats.…”

Section: Methodsmentioning

confidence: 99%

“…To determine whether the reduction of FFA and TG affects either the oral glucose tolerance test (OGTT) [15] or the intravenous insulin test (IVIT) [15], 2 new groups of pregnant animals were studied, one treated with acipimox (80 mg) and the other with distilled water, as described above for experiment 1. On day 20 of pregnancy, and after a fasting period of 12 hours, an OGTT was performed 3 hours after the administration of acipimox or distilled water, time of maximum decrease in FFA and TG, by administering 2 g glucose/kg body weight dissolved in distilled water by gavage.…”

Section: Methodsmentioning

confidence: 99%

Effect of Acipimox on Plasma Lipids and Glucose/Insulin in Pregnant Rats

Sánchez-Vera

Bonet

Viana

et al. 2002

Journal of Diabetes Research

View full text Add to dashboard Cite

To determine how a reduction in maternal hypertriglyceridemia during late pregnancy may affect glucose/insulin relationships, pregnant and virgin rats were orally treated with acipimox, a potent antilipolytic agent. In 20-day pregnant rats receiving 80 mg of acipimox, plasma triglycerides (TG), free fatty acids (FFA), and glycerol decreased more than in virgin rats shortly after the drug (up to 7 hours), when compared with animals treated with distilled water, whereas plasma glucose level was unaffected by the treatment in either group of rats. When acipimox was given every 12 hours from day 17 to day 20 of pregnancy, plasma TG, FFA, and glycerol levels progressively increased, whereas they either decreased or did not change in virgin rats receiving the same treatment, with no effect in plasma glucose levels in either group. Fetal body weight was lower than in controls in 20-day pregnant rats that received acipimox for 3 days. On day 20 of pregnancy, 3 hours after receiving acipimox or distilled water, rats received a 2 g glucose/kg oral load and it was found that the change in plasma glucose was similar in both groups, whereas the increase in plasma insulin was greater in pregnant rats treated with acipimox. However, no difference was found in either variable after the oral glucose load in virgin rats receiving acipimox or distilled water. No differences in plasma glucose levels were found after intravenous (IV) administration of insulin in pregnant rats treated or not treated with acipimox. In conclusion, present results show that administration of acipimox during the last days of gestation inhibited lipolysis and decreased fetal weight. Over a short period of time, in pregnant rats, reductions of plasma FFA and TG after acipimox treatment improved the glucose-induced insulin release, but did not seem to have any effect in peripheral insulin resistance. The enhanced lipolytic activity present during late gestation gives rise to an elevation in plasma free fatty acids (FFA) and triglycerides (TG), both in women and rats [1][2][3]. Some tissues use fatty acids as fuel, sparing glucose for the fast-growing fetus and those maternal tissues that can only use glucose as fuel energy [4]. The mechanisms involved in this elevated lipolytic activity are uncertain, but the rising levels of placental lactogen and the insulin resistance during late pregnancy seem to play a relevant role [5][6][7].The enhanced availability of FFA to the liver seems to contribute to the increased production of TG by this organ [8] and therefore to the development of maternal hypertriglyceridemia. Exaggerated increment of TG in maternal circulation may be involved in some of the pregnancy-induced complications, including eclampsia [9] and insulin resistance that would cause the development of gestational diabetes [7], 2 of the most common pregnancy-induced complications. Therefore, decreasing the hypertriglyceridemia of late pregnancy may be of therapeutic use. Nevertheless, this therapeutic approach may not be risk free for the fetus, becaus...

show abstract

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

Cited by 32 publications

References 21 publications

Role of 17beta-estradiol and/or progesterone on insulin sensitivity in the rat: implications during pregnancy

Role of 17beta-estradiol and/or progesterone on insulin sensitivity in the rat: implications during pregnancy

Correlation of serum leptin and insulin levels of pregnant protein-restricted rats with predictive obesity variables

Effect of Acipimox on Plasma Lipids and Glucose/Insulin in Pregnant Rats

Contact Info

Product

Resources

About