nutrient

Metabolism

LOUISE

LAIÕOUE,2 SANDRA

MINIACI3 AND KRISTIHE

G. KOSKI4

School of Dietetics and Human Nutrition, McGill University, Ste. Anne de Bellevae, Qué.,Canada, H9X 3V9 increased postnatal mortality (Koski et al. 1986, Koski and Hill 1986). Diet-induced changes in placental composition were not evaluated in these earlier studies. Maternal malnutrition has been shown to interfere with normal placental growth as reflected by reduced weight, protein and DNA content measured in placentas of pregnant rats fed low protein diets throughout gestation (Hastings-Roberts and Zeman 1977, Wunderlich et al. 1979). Dams fed these low protein diets were also shown to have reduced placental transport of analogues of amino acids and glucose (Rosso 1981), suggesting that reduced placental size in response to maternal malnutrition may have resulted in a reduced area for maternal-fetal exchange of nutrients and contributed to the intrau terine growth retardation seen in protein-energy mal nutrition. The specific effects of maternal dietary glucose restriction on placental development have not been extensively studied, even though glucose is the prin cipal metabolic fuel for the developing placenta. The placenta has a higher metabolic rate per unit weight at term (Battaglia 1989) and a higher rate of glucose utilization than the fetus, and close to 2/3 of the glucose delivered to the fetoplacental unit is metabo lized by the placenta to sustain its growth and metab olism (Hay 1991). Furthermore, recent investigations have indicated that dietary glucose restriction can

ABSTRACT In this study we investigated whether placenta! glycogen reserves and protein and DMA content could be manipulated by altering the level of glucose in the maternal diet. Pregnant rat dams were fed isocaloric diets containing graded levels of glucose (0, 12, 24 and 60%), and placentas were analyzed for glycogen, protein and DNA content on gestational days 18.5 to 21.5. Regardless of the level of glucose in the maternal diet, there was a significant increase in placenta! size with advancing age, which was charac terized by protein accretion but not by an increase in cell number or glycogen content. Restriction of glucose in the diets of pregnant dams failed to produce statistically significant reductions in placental protein, DNA and glycogen and did not retard placental growth, even though intrauterine growth retardation was observed. Fetal weight, plasma glucose, and liver and heart glycogen were positively correlated with placental weight and inversely correlated with placental glycogen and DNA concentrations; by contrast, no significant correla tions were calculated between maternal and placental variables. Our study indicates that the placenta is not affected by a specific dietary glucose restriction and that changes in placental weight or glycogen content do not account for the growth retardation observed in fetuses of dams fed glucose-restricted diets. J. Nutr. 122: 2374-2382, 1992. INDEXING KEY WORDS: •placenta •glycogen •protein •DNA

rats

Adequate nutrient supply to the fetus during gestation, particularly of glucose, which is the main substrate of fetal and placental metabolism, has been recognized as an important determinant of pregnancy outcome (Battaglia 1989, Hay 1991). Recent investiga tions have shown that restriction in the intake of dietary glucose or glucose precursors by pregnant rat dams was associated with intrauterine growth retardation, decreased fetal liver glycogen stores and 0022-3166/92

$3.00 ©1992 American

Institute

of Nutrition.

'Supported by a grant from the Natural Sciences and En gineering Research Council of Canada (NSERC 3625). 2L. Lanoue was a recipient of Fonds pour la Formation des Chercheurs et l'Aide à la Recherche (FCAR|, a Québecprovincial postgraduate scholarship. 3S. Miniaci received a Natural Science and Engineering search Council (NSERC I of Canada Summer Undergraduate search Scholarship. 4To whom correspondence should be addressed.

Received 28 February 1992. Accepted 5 August 1992. 2374

Re Re

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Placental Composition Does Not Respond to Changes in Maternal Dietary Carbohydrate Intake in Rats1

PLACENTA

COMPOSITION

MATERIAL AND METHODS Experimental design. In this experiment, the ef fects of graded levels of dietary carbohydrate (0, 12, 24 and 60% glucose) fed throughout pregnancy were studied in rats during the last 4 d of gestation (gd 18.5-21.5) in a 4 x 4 factorial design. Impregnated Sprague-Dawley rats weighing 180-220 g were pur chased from Charles River Canada (St-Constant, Qué.)and received within 2 d of mating. Gestational day 0 (gd 0) was defined as the day following the overnight mating. Impregnated dams were fed com mercial nonpurified diet during gd 0 and 1 until they were housed individually in wire-suspended, stainless steel cages in a temperature-controlled room (22°C) with a 12-h light cycle (0700-1900 h), at which time experimental diets and water were given ad libitum. The animals were randomly assigned to one of the 16 experimental groups. Food intake and body weight were recorded every second day. Experimental diets. The compositions of the control (60% glucose), carbohydrate-restricted (12 and 24% glucose) and carbohydrate-free (0% glucose) diets are given in Table 1. The glucose concentrations of the experimental diets were based on previous work done by Koski et al. (1986) and Koski and Hill (1986). However, in this experiment a previously untested diet was fed to the dams,- the effects of a 24% glucose diet during pregnancy was investigated because it was previously shown that fetuses from dams fed 12% glucose accumulated significantly less liver glycogen

DIET

2375

than fetuses from control dams, thereby suggesting that this level of carbohydrate was not adequate when fetal liver glycogen concentration was used to evaluate dietary adequacy. All diets were isocaloric and supplied 17.4 kj of metabolizable energy per gram of dry matter as recommended for pregnant rats (NRC 1978). Glucose was the main source of energy in the control diet. Restriction of this nutrient in the ex perimental diets was done by isoenergetic substi tution of soybean oil for glucose. These low carbohy drate, triacylglycerol-rich diets provide glycerol, which can act as a glucose precursor, and intact triglycéride has been calculated to contribute 10% glucose equivalents from the glycerol moiety by weight; thus, the 40% fat found in our glucose-free diet provided the 4% carbohydrate that has been found essential for pregnancy to be carried to term in rats (Koski et al. 1986). Casein contributed -10% of the total energy supply. The amount of casein added to the diets was calculated to provide 9.5% protein, which was previously determined (Koski et al. 1986) to be the lowest level of protein required to supply the adequate amounts of nitrogen and essential amino acids during rat pregnancy for optimal fetal growth and to prevent excess protein being transformed to glucose via gluconeogenesis. Sample collection and analysis. Dams were killed in the fed state between 0700 and 1200 h following anesthesia with ketamine-HCL (Rogarsetic, 30 mg/kg, Rogar/STB, London, Ont.) in the neck region to min imize fetal anesthesia. Maternal blood was withdrawn by cardiac puncture. All procedures were conducted in conformance with guidelines for experimental procedures set forth by the local animal care com mittee of McGill University and by the Canadian Council on Animal Care (1984). A caesarian section was performed and fetal blood samples were collected into heparinized capillary tubes from severed axillary vessels of fetuses still attached to their respective placenta. Immediately after blood collection, the livers and hearts of fetuses were removed and rapidly frozen at -80°C by immersion in liquid nitrogen. Maternal livers were excised from the abdominal cavity and freeze-clamped in liquid nitrogen. The uterus of each dam was examined for implantation and résorptionsites. Resorption sites, in utero deaths and live fetuses were expressed as a percentage of implantation sites. The placentas of fetuses were re moved, weighed and freeze-clamped in liquid nitrogen. The placentas were stored individually at -80°C until analyzed. Maternal and fetal plasma glucose were measured by an enzymatic colorimetrie reaction using an Abbott VP Super System Analyzer (Irving, TX) with a Sigma kit (Sigma Chemical, St. Louis, MO). Maternal and fetal plasma insulin and glucagon concentrations were determined in duplicate by RIA (Biodata, NCS Diagnostics, Mississauga, Ont). For the glucagon

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reduce total placental glycogen content in rats at d 19.5 of pregnancy (Koski and Mancini 1990). Placental glycogen has been postulated to be an energy source to support placental metabolic activities (Beaconsfield and Ginsburg 1979) and to sustain amino acid transfer during hypoxia (Longo et al. 1973) as well as to maintain the vasomotor functions of the placental blood vessels (Hytten 1978). It has also been proposed that placental glycogen can be used as a general indi cator of placental metabolism (Rosso et al. 1976), which in turn is one important determinant of fetal growth. However, a direct contribution of placental glycogen to the fetus remains speculative. The present study was designed to answer the fol lowing questions: 1} does restriction of maternal di etary glucose intake compromise placental growth as measured by DNA and protein content? 2) is placental glycogen, like other maternal and fetal glycogen reserves, affected by maternal dietary glucose manipulation? If these placental variables are affected by dietary glucose, we could suggest that the negative consequences of maternal dietary glucose restriction on fetal growth and development are in part mediated by changes in placental growth and metabolism.

AND MATERNAL

LANGUE ET AL.

2376

TABLE 1 Composition of control and carbohydrate-restricted diets1 Glucose level 0%

Ingredient

12%

24%

60%

mix6Mineral mix7DL-MethionineSodium bicarbonateWeight, gMetabolizable

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Glucose2Soybean oil3Cellulose4Casein5Vitamin

energy, kj/g039.6441.36111.25.50.341.00100.0417.4Õ1234.9134.09111.25.50.341.00100.0417.4;•2430.1826.82111.25.50.341.00100.0417.46016.005.0 'Dry weight basis (grams). ^Dextrose (anhydrous), ICN Biochemicals Canada, Montréal,Qué. ^Degummed soybean oil, Canadas Packers, Montréal,Qué. 4Alphacel, ICN Biochemicals Canada. 5High nitrogen casein (ICN Biochemicals Canada), containing 86.5% protein (N x 6.25) or 89.1% protein (N x 6.71). 6Vitamin mixture supplied the following (mg/kg diet): niacin, 100; calcium pantothenate, 32; riboflavin, 12; pyridoxine hydrochloride, 24; thiamin hydrochloride, 16; folacin, 4; biotin, 1; cyanocobalamine, 0.2; all-rac-a-tocopheryl acetate, 60; menaquinone, 0.6; choline chloride, 4000; cholecalciferol 0.039; retinyl palmitate, 2.75. 7Mineral mixture supplied the following (g/kg diet): CaHPO4, 26.44; KHCO3, 20.35; NaCl, 2.82; MgSO4, 4.38; CrK(SO4)2-12H2O, 0.0064; CuCO3-Cu(OH)2-H2O, 0.0198; KIO3, 0.0006; FeSO4.7H2O, 0.3931; MnCO3, 0.1046; ZnCO3, 0.1726; Na2SeO3, 0.0005; NaMoO4-2H2O, 0.0177; KF-2H2O, 0.0111.

assay, blood was collected with a proteinase inhibitor (Trasylol, Miles Laboratories, Etobicoke, Ont). Glycogen in fetal heart and liver and maternal liver was measured according to the method described by Lo et al. (1970). Within each litter one third of the placentas was assayed for glycogen (Lo et al. 1970). A random subset was taken from the remaining placentas and homogenized in phosphate buffer for the analyses of protein and DNA. Placental protein was measured by the method of Hartree (1972), which is a modified Lowry assay; DNA was measured by the diphenylamine method as modified by Burton (1956). Protein and DNA assays were done in duplicate. Glycogen, protein and DNA concentration values were converted to total placental content by mul tiplying milligrams per gram of wet weight by the corresponding placental weight. Cell number was es timated by dividing total DNA content of the placenta by 6.2, which is the amount of DNA con tained per diploid cell of the rat (Winick and Noble 1965). The protein and glycogen content per cell was estimated according to the following formula described by Winick and Noble (1965): pg per cell = total content (g) x HP/cell number (IO6). This paper reports only the measurements done on placental tissue. Other maternal and fetal variables, although measured on the same experimental animals, will be reported elsewhere,- relevant correlations are included here.

Statistical analysis. Placental glycogen, protein and DNA content were assayed on individual tissues. The data were tested against dietary treatment (main effect of diet: 0, 12, 24 and 60% glucose) and de velopment (main effect of age: gd 18.5, 19.5, 20.5 and 21.5) and their interaction by a two-way nested ANOVA with the error term attributed to the dams of each litter and not to the individual placentas because the dams were the experimental units (Freund et al. 1986). Significant differences among groups were tested by least square means. The nested design not only tested for the main effects of diet and gestational age on the dependent variables, but also controlled for the variations among dams caused by differences in food intake or weight gain. In this study, ANOVA without nesting the placental data by dams resulted in a significant dietary effect on placental protein content (P < 0.04) and a significant interaction of diet and development on placental glycogen (P < 0.008). These effects were no longer statistically significant when the data were analyzed using a nested model, indicating that there was high variability within each litter. In the absence of any statistically defined inter action between diet and development, the data were pooled and analyzed for main effects. In such case, Schefféor contrasts were the a posteriori tests used to establish significant differences (P < 0.05) between groups. Pearson correlation coefficients were cal culated between placental, maternal and fetal

PLACENTA dietary carbohydrate o% 450

12%

COMPOSITION

content 24%

I

AND MATERNAL

15

DIET

fetal weight/placenta!

2377

weight

I 60%

grams

grams

4.5

12

b c 3.6

270

2.7

180

1.8

90

0.9

0

0.0 food intake

weight gain

weight fetal

maternal

weight placenta)

FIGURE 1 The effects of dietary glucose on maternal food intake and weight gain and on fetal and placental weights. Bars represent means ±SEM pooled over gestational day (gd) 18.5 to 21.5; n = 35-45 dams/diet group, n = 475-535 fetuses/diet group. Bars with different superscripts indicate significant effect of dietary glucose levels as deter mined by ANOVA (P < 0.0001) and by least square means (P < 0.05).

measurements in response to diet over d 18.5 to 21.5 of gestation. All statistics were performed using SAS (Freund et al. 1986).

RESULTS Food intake and reproductive performance As shown in Figure 1, restriction of glucose in the maternal diet was associated with a significant reduction in cumulative food intake (ANOVA, P < 0.0001) and maternal weight gain (ANOVA, P < 0.0001) during pregnancy. There were no differences in the number of implantation sites and in utero death rates among the different dietary groups (data not shown). However, dams fed glucose-free diets had significantly higher résorption frequency (9.7%) than dams fed glucose-containing diets (5.5%, 12% glucose, P < 0.005; 4.9%, 24% glucose, P < 0.006; 3.9%, 60% glucose, P < 0.002). This resulted in a significantly smaller percentage of live fetuses in the glucose-free group (90%) following delivery by caesarian section compared with the other dietary groups (94%, 12% glucose, P < 0.009; 95%, 24% glucose, P < 0.001; 96%, 60% glucose, P < 0.004).

Placental characteristics Dietary effects. Low levels of glucose in the maternal diet throughout pregnancy (0 and 12%

18.5

19.5 20.5 gestational days

21.5

FIGURE 2 Fetal to placental weight ratio in dams fed glucose-free diet (solid bars, n = 128-142 ratios/gestational day) and in dams fed glucose-containing diets (hatched bars, n = 286-450 ratios/gestational day). Bars represent means ± SEM. Bars with different superscripts indicate significant difference between dams fed glucose-free diet and dams fed glucose-containing diets as determined by ANOVA (P < 0.0001) and contrasts (P < 0.05).

glucose) were associated with significantly reduced fetal weights during the last 4 d of gestation (ANOVA, P < 0.001), whereas placental weights were not affected (ANOVA, P < 0.20, Fig. 1). The effects of dietary glucose restriction with advancing gestational age were most severe in dams fed glucose-free diets compared with glucose-fed dams, resulting in a sig nificantly lower fetal to placental weight ratio during gd 20.5 and 21.5 (ANOVA, P < 0.0001, Fig. 2). Maternal dietary glucose concentration had no sig nificant effects on placental weight or glycogen, protein and DNA content. Consequently, the data from the four dietary groups were pooled and tested as one group for developmental effects. Developmental effects. Placental growth during the last 4 d of gestation was assessed by weight, cell number, and protein and DNA content (Table 2 and Fig. 3 and 4). The placentas increased significantly in size from gd 18.5 to 21.5 (ANOVA, P < 0.0001, Table 2); this increased weight did not result from hyperplasia because there was no concomitant increase in cell number during this period (Table 2). In fact, placental cell number was significantly reduced in placentas at gd 21.5 (P < 0.003, Table 2) compared with those at gd 18.5 and gd 19.5. Thus cell division stopped in the placenta by gd 18.5 as reflected by the significant decrease in total DNA content (ANOVA, P < 0.01, Fig. 4) and concentration (ANOVA, P < 0.0001,

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360

2378

LANGUE ET AL. [qestational

days'

gestational days 18.5

20.5

19.5

18.5

21.5 ba»a

100

50

I

I

Ì 21.5

1.2

40

0.9

30

•06 a.

20

0>

25

75>

0 GLYCOGEN

DNA

0.3

10

E

PROTEIN

0.0

GLYCOGEN

DNA

PROTEIN

FIGURE 3 Glycogen, protein and DNA concentration of placentas from rats fed 0, 12, 24 and 60% glucose diets. Bars represent means ±SEM; n = 107-155 placentas/d for glycogen, n = 88-174 placentas/d for DNA, n = 105-199 placentas/d for protein. Superscripts indicate significant differences between gestational days as determined by ANOVA (P < 0.001) and contrasts (P < 0.05).

FIGURE 4 Glycogen, protein and DNA content of placentas from rats fed 0, 12, 24 and 60% glucose diets. Bars represent means ± SEM; n = 107-155 placentas/d for glycogen, n = 88-174 placentas/d for DNA, n = 105-199 placentas/d for protein. Superscripts indicate significant differences between gestational days as determined by ANOVA (P < 0.001) and contrasts (P < 0.05).

Fig. 3), whereas cell enlargement occurred during gd 18.5 to 20.5 as reflected by the significant increase in total placental protein (ANOVA, P < 0.0001, Fig. 4) and placental cell protein content (ANOVA, P < 0.002, Table 2). Gestational days 18.5 to 20.5 were characterized by protein accretion in the placenta (Fig. 4), and these changes in protein content paralleled the increase in placental weight during the same period. From gd 20.5 to 21.5, the nonsignificant increase in placental weight was not supported by greater protein content per cell (Table 2) or per placenta (Fig. 4) and may indicate changes in water or lipid content of the tissue. Placental metabolism as assessed by changes in glycogen levels showed that glycogen concentration (Fig. 3) and total glycogen content per placenta (Fig. 4) were significantly reduced on gd 20.5 and 21.5 com pared with gd 18.5 and 19.5 (P < 0.0001). At term, placental glycogen was markedly depleted as cellular content was reduced by 30% relative to gd 18.5 (Table 2). Changes in placental glycogen content were in dependent of placental size during the study period. Correlations. Placental weight changes between gd 18.5 to 21.5 were positively correlated with total protein per placenta (r = 0.63, P < 0.0001) with protein content per cell (r = 0.48, P < 0.0001) but not with placental glycogen or DNA content. Placental glycogen and DNA, however, were inversely cor related with placental protein content (r = -0.30, P < 0.0002 and r = -0.65, P < 0.0001, respectively). No significant correlations were calculated be tween maternal plasma glucose, insulin, glucagon and liver glycogen and placental weight, protein, DNA and glycogen content (as milligrams per gram of wet weight or as milligrams per total tissue). By contrast, as shown in Table 3, fetal weight, plasma insulin,

glucagon, glucose, and liver and heart glycogen were positively correlated between gd 18.5 to 21.5 with placental weight and inversely correlated with placental glycogen concentration. Placental DNA but not protein concentrations were negatively correlated with fetal weight, plasma glucose and glucagon con centrations and liver and heart glycogen between gd 18.5 to 21.5. Variations in total placental protein during gd 18.5 to 21.5 were positively correlated with changes in fetal weight, plasma insulin and liver and heart glycogen, whereas placental total glycogen content was negatively correlated with all fetal vari ables measured except plasma insulin. Fetal weight and fetal plasma glucose were negatively correlated with placental DNA content (Table 3).

DISCUSSION In this study we investigated whether the absence of glucose in the maternal diet could alter placental growth and development. In contrast to proteinenergy malnutrition, which has been shown to com promise placental weight (Hastings-Roberts and Zeman 1977), maternal dietary glucose restriction throughout pregnancy did not compromise placental growth. Because placental weight gain results from successive stages of hyperplasia and hypertrophy, DNA and protein content were measured, but neither responded to changes in maternal dietary glucose intake. As shown by the developmental changes in placental DNA and protein content measured in our study, and in accordance with previous reports on placental development (Butterstein and Leathern 1974, Winick and Noble 1965), by gd 18.5 cell di vision had stopped whereas protein synthesis con-

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75

20.5

19.5

PLACENTA

COMPOSITION

AND MATERNAL

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2379

TABLE 2 Placenta! weight, cell number and glycogen and protein cell content during the last 4 d of gestation Gestational

'Values significantly 2Results 3Results 4Results 5Results

0.335 (85) 134.7 (26) 7.62 (85) 225.3

±0.004a 0.388 (141) 132.9 ±2.6b (36) 8.36 ±0.42b ±6.69a19.5(285) (141) 277.9

day

±0.004b 0.402 ±2.3b (172) 126.2 ±0.41b (42) 7.32 ±5.95b20.5(357) (172) 311.6

are means ±SEM, with number of determinations in parentheses. Values within different (P < 0.05) as determined by Scheffétest. from ANOVA: main effect of diet (P < 0.20); main effect of age (P < 0.001). from ANOVA: main effect of diet (P < 0.13); main effect of age \P < 0.01). from ANOVA: main effect of diet (P < .86); main effect of age (P < 0.0001). from ANOVA: main effect of diet [P < 0.63); main effect of age (P < 0.0001).

tinued until near term (gd 20.5). Gestational days 18.5 to 20.5 are characterized by active protein deposition, and this hypertrophie phase of growth has been as sociated with an increased ability of the placenta to transfer nutrients to the fetus (Rosso et al. 1976); this rise in placental protein near term was also not af fected by dietary glucose restriction. The absence of any effect of dietary glucose restriction on placental DNA and protein between gd 18.5 and 21.5 may have been caused by the absence of cell division during that period, although glucose restriction was imposed from the first day of pregnancy. Thus, dietary glucose may not be the limiting factor for placental de velopment as long as the energy demands of the pregnant dams are met by the diet. By contrast, protein-depleted diets have been shown to interfere with placental growth as reflected by lower placental weight, reduced DNA and protein content in placentas of dams fed diets containing 4 or 5% casein compared with dams fed diets containing 18% casein or more (Hastings-Roberts and Zeman 1977, Wun derlich et al. 1979). However, pair-feeding studies to control for the lowered food intake of protein-defi cient dams have shown that the energy deficit was involved in the reduced growth rate observed in placentas from these dams (Hastings-Roberts and Zeman 1977). A strong relationship has been shown between fetal and placental weight in sheep, guinea pigs and humans (Gilbert and Leturque 1982, Hay 1991, Pivalizza et al. 1990). As a consequence, it has been generally assumed that the factors that affect placental growth are also determinants of fetal growth (Rosso 1981) and vice versa. Results from the present investigation in conjunction with results from previous studies using dietary glucose as the limiting nutrient failed to support this observation. We have shown that dietary glucose restriction resulted in in trauterine growth retardation, increased number of

±0.003bc 0.415 ±1.7ab (159) 121.7 ±0.40b (42) 5.42 ±5.83C21.5(324) (159) 299.9 a row having different

±0.004C ±2.2a ±0.17a ±5.78bc

superscripts

are

résorptions and reduced percentage of live pups but did not impair placental growth. Using a similar di etary model, Fergusson and Koski (1990) also ob served impaired reproductive performance and fetal growth in offspring born to dams fed glucose-free diets without any change in placental weight; placental composition was not evaluated. A brief review of the current literature showed that fetal weight changes have not been consistently correlated with corresponding placental weight changes. The sig nificant correlation calculated between fetal and placental weights in this study most likely reflected the effect of growth between gd 18.5 and 21.5 rather than any dietary effect. Gilbert and Leturque (1982), Jansson and Persson (1990), Jones et al. (1988) and Pivalizza et al. (1990) reported significantly reduced placental weight during intrauterine growth retardation, whereas Lawrence et al. (1989) and Nitzan et al. (1979) observed greater growth re striction in fetuses than in placentas after uterine artery ligation. There have been other cases in which fetal but not placental weight was significantly af fected by treatments such as maternal food depri vation (Gilbert and Leturque 1982) and maternal dia betes (Gewolb et al. 1983). Part of these discrepancies can be attributed to the differences in research design, nature of the species, severity of the insult and the gestation period examined. Jones et al. (1988) sug gested that fetal hypoglycemia is an important deter minant of placental growth, because fetal blood glucose has been shown to contribute to a certain degree of placental glucose requirements. Dams and fetuses from glucose-restricted groups using our di etary model have been shown to have plasma glucose concentrations similar to that observed in control groups (Fergusson and Koski 1990). The profile of placental glycogen in this study com pared favorably with the observation that there is a progressive depletion of placental glycogen as term

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Weight,2 g Cells3 |106) Glycogen,4 pg/cell Protein,5 pg/cell18.5|208)

in rats1

2380

LANGUE

ET AL.

TABLE 3 Correlations

between placental

weight, glycogen, protein and DNA and fetal weight, plasma insulin, glucagon, glucose and liver and heart glycogen1 Fetal variables

wt)Liver1590.410.0001154-0.440.0001157NSNS150-0.370.000115 (mg/g wet Downloaded from https://academic.oup.com/jn/article-abstract/122/12/2374/4754672 by University of Rhode Island user on 16 October 2018

PlacentalvariablesWeight

in1560.330.0001151-0.280.000 (g)Glycogen

wt)Protein, (mg/g wet

wt|DNA (mg/g wet

wt)Glycogen (mg/g wet

(mg/tissue)Protein

(mg/tissue]DNA

(mg/tissue)'n

ofnrPnrPnrPnrPnrPnrPnrPmeasurements;measurements represents number coefficient0, represents Pearson correlation 21diets; over gd 18.5 to two0.05); between NS = not [P

Placental composition does not respond to changes in maternal dietary carbohydrate intake in rats.

In this study we investigated whether placental glycogen reserves and protein and DNA content could be manipulated by altering the level of glucose in...
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