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The intrauterine and nursing period is a window of susceptibility for development of obesity and intestinal tumorigenesis by a high fat diet in Min/+ mice as adults.

Ngo HT, Hetland RB, Steffensen IL - J Obes (2015)

Bottom Line: We studied how obesogenic conditions during various life periods affected obesity and intestinal tumorigenesis in adult C57BL/6J-Min (multiple intestinal neoplasia)/+ mice.In the glucose tolerance test, the early exposure to a 45% fat diet in utero, during nursing, or during both in utero and nursing, did not affect blood glucose, whereas a 45% fat diet given to adults or throughout life did.The intrauterine and nursing period is a window of susceptibility for dietary fat-induced obesity and intestinal tumor development.

View Article: PubMed Central - PubMed

Affiliation: Department of Food, Water and Cosmetics, Division of Environmental Medicine, Norwegian Institute of Public Health, P.O. Box 4404 Nydalen, 0403 Oslo, Norway.

ABSTRACT
We studied how obesogenic conditions during various life periods affected obesity and intestinal tumorigenesis in adult C57BL/6J-Min (multiple intestinal neoplasia)/+ mice. The mice were given a 10% fat diet throughout life (negative control) or a 45% fat diet in utero, during nursing, during both in utero and nursing, during adult life, or during their whole life-span, and terminated at 11 weeks for tumorigenesis (Min/+) or 23 weeks for obesogenic effect (wild-type). Body weight at 11 weeks was increased after a 45% fat diet during nursing, during both in utero and nursing, and throughout life, but had normalized at 23 weeks. In the glucose tolerance test, the early exposure to a 45% fat diet in utero, during nursing, or during both in utero and nursing, did not affect blood glucose, whereas a 45% fat diet given to adults or throughout life did. However, a 45% fat diet during nursing or during in utero and nursing increased the number of small intestinal tumors. So did exposures to a 45% fat diet in adult life or throughout life, but without increasing the tumor numbers further. The intrauterine and nursing period is a window of susceptibility for dietary fat-induced obesity and intestinal tumor development.

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Related in: MedlinePlus

Nonfasted blood glucose levels (mmol/L, mean ± SD) for (a) Min/+ mice; females at 6 and 11 weeks and males at 6 and 11 weeks, (b) wild-type mice; females at 6 and 23 weeks and males at 6 and 23 weeks, shown for both genotypes with columns in white, light grey, dark grey and black color, respectively. P = PhIP. The experimental groups are as explained in the legend to Figure 1. n = 9–46.
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fig7: Nonfasted blood glucose levels (mmol/L, mean ± SD) for (a) Min/+ mice; females at 6 and 11 weeks and males at 6 and 11 weeks, (b) wild-type mice; females at 6 and 23 weeks and males at 6 and 23 weeks, shown for both genotypes with columns in white, light grey, dark grey and black color, respectively. P = PhIP. The experimental groups are as explained in the legend to Figure 1. n = 9–46.

Mentions: To test the hypothesis that obesity may affect intestinal tumorigenesis by disturbing the blood glucose regulation, blood glucose levels (nonfasted) were measured in all mice. This was done at weeks 6 and 11 in the Min/+ mice (Figure 7(a)), and at weeks 6 and 23 in the wild-type mice (Figure 7(b)). When compared at 6 weeks, the Min/+ mice had higher levels of blood glucose than the wild-type mice (P < 0.001), which was also found in our previous experiments (see [33], Ngo et al., 2014; unpublished results). The blood glucose levels were significantly higher in male compared with female Min/+ mice, at both 6 and 11 weeks, and in wild-type mice, at both 6 and 23 weeks, and in mice treated with PhIP or not (P < 0.001 all comparisons). It was also seen in all dietary groups for both time points together (P < 0.001 for all comparisons). The blood glucose results are presented for females and males separately (Figure 7).


The intrauterine and nursing period is a window of susceptibility for development of obesity and intestinal tumorigenesis by a high fat diet in Min/+ mice as adults.

Ngo HT, Hetland RB, Steffensen IL - J Obes (2015)

Nonfasted blood glucose levels (mmol/L, mean ± SD) for (a) Min/+ mice; females at 6 and 11 weeks and males at 6 and 11 weeks, (b) wild-type mice; females at 6 and 23 weeks and males at 6 and 23 weeks, shown for both genotypes with columns in white, light grey, dark grey and black color, respectively. P = PhIP. The experimental groups are as explained in the legend to Figure 1. n = 9–46.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4383426&req=5

fig7: Nonfasted blood glucose levels (mmol/L, mean ± SD) for (a) Min/+ mice; females at 6 and 11 weeks and males at 6 and 11 weeks, (b) wild-type mice; females at 6 and 23 weeks and males at 6 and 23 weeks, shown for both genotypes with columns in white, light grey, dark grey and black color, respectively. P = PhIP. The experimental groups are as explained in the legend to Figure 1. n = 9–46.
Mentions: To test the hypothesis that obesity may affect intestinal tumorigenesis by disturbing the blood glucose regulation, blood glucose levels (nonfasted) were measured in all mice. This was done at weeks 6 and 11 in the Min/+ mice (Figure 7(a)), and at weeks 6 and 23 in the wild-type mice (Figure 7(b)). When compared at 6 weeks, the Min/+ mice had higher levels of blood glucose than the wild-type mice (P < 0.001), which was also found in our previous experiments (see [33], Ngo et al., 2014; unpublished results). The blood glucose levels were significantly higher in male compared with female Min/+ mice, at both 6 and 11 weeks, and in wild-type mice, at both 6 and 23 weeks, and in mice treated with PhIP or not (P < 0.001 all comparisons). It was also seen in all dietary groups for both time points together (P < 0.001 for all comparisons). The blood glucose results are presented for females and males separately (Figure 7).

Bottom Line: We studied how obesogenic conditions during various life periods affected obesity and intestinal tumorigenesis in adult C57BL/6J-Min (multiple intestinal neoplasia)/+ mice.In the glucose tolerance test, the early exposure to a 45% fat diet in utero, during nursing, or during both in utero and nursing, did not affect blood glucose, whereas a 45% fat diet given to adults or throughout life did.The intrauterine and nursing period is a window of susceptibility for dietary fat-induced obesity and intestinal tumor development.

View Article: PubMed Central - PubMed

Affiliation: Department of Food, Water and Cosmetics, Division of Environmental Medicine, Norwegian Institute of Public Health, P.O. Box 4404 Nydalen, 0403 Oslo, Norway.

ABSTRACT
We studied how obesogenic conditions during various life periods affected obesity and intestinal tumorigenesis in adult C57BL/6J-Min (multiple intestinal neoplasia)/+ mice. The mice were given a 10% fat diet throughout life (negative control) or a 45% fat diet in utero, during nursing, during both in utero and nursing, during adult life, or during their whole life-span, and terminated at 11 weeks for tumorigenesis (Min/+) or 23 weeks for obesogenic effect (wild-type). Body weight at 11 weeks was increased after a 45% fat diet during nursing, during both in utero and nursing, and throughout life, but had normalized at 23 weeks. In the glucose tolerance test, the early exposure to a 45% fat diet in utero, during nursing, or during both in utero and nursing, did not affect blood glucose, whereas a 45% fat diet given to adults or throughout life did. However, a 45% fat diet during nursing or during in utero and nursing increased the number of small intestinal tumors. So did exposures to a 45% fat diet in adult life or throughout life, but without increasing the tumor numbers further. The intrauterine and nursing period is a window of susceptibility for dietary fat-induced obesity and intestinal tumor development.

Show MeSH
Related in: MedlinePlus