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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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The number of small intestinal tumors for pooled male and female Min/+ mice (mean ± SD). Two separate experimental groups receiving a 45% fat diet during in utero and nursing period or throughout life were injected with PhIP (marked P). The experimental groups are as explained in the legend to Figure 1. n = 44–65. aSignificantly different from the negative control group given a 10% fat diet throughout life. bSignificantly different from the group given a 45% fat diet throughout life. cSignificantly different from the group given a 45% fat diet in utero and during nursing. dSignificantly different with PhIP compared with no PhIP exposure in the groups given a 45% fat diet during in utero and nursing period. eSignificantly different with PhIP compared with no PhIP exposure in the groups given a 45% fat diet throughout life. n.s. = not significantly different.
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fig9: The number of small intestinal tumors for pooled male and female Min/+ mice (mean ± SD). Two separate experimental groups receiving a 45% fat diet during in utero and nursing period or throughout life were injected with PhIP (marked P). The experimental groups are as explained in the legend to Figure 1. n = 44–65. aSignificantly different from the negative control group given a 10% fat diet throughout life. bSignificantly different from the group given a 45% fat diet throughout life. cSignificantly different from the group given a 45% fat diet in utero and during nursing. dSignificantly different with PhIP compared with no PhIP exposure in the groups given a 45% fat diet during in utero and nursing period. eSignificantly different with PhIP compared with no PhIP exposure in the groups given a 45% fat diet throughout life. n.s. = not significantly different.

Mentions: All mice had small intestinal tumors (adenomas), independent of dietary or carcinogenic exposures, confirming 100% incidence of small intestinal tumors as is commonly found in the Min/+ mice [25–27, 33]. The number of small intestinal tumors was not significantly different between the genders, thus the data for males and females are presented together (Figure 9). Although slightly increased, exposure to the 45% fat diet only in utero did not significantly increase the number of small intestinal tumors compared with the negative control group given a 10% fat diet throughout life. Exposure to a 45% fat diet only during the nursing period was significantly increased compared with the negative control group (P < 0.05). However, exposure to a 45% fat diet both in utero and during nursing, significantly increased the number of small intestinal tumors further, compared with the negative control group (P < 0.05), and compared with a 45% diet only in utero (P < 0.05), but not compared with only during nursing. Thus the effect of a 45% fat diet during the nursing period is more efficient in increasing the tumor number than the exposure in utero.


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)

The number of small intestinal tumors for pooled male and female Min/+ mice (mean ± SD). Two separate experimental groups receiving a 45% fat diet during in utero and nursing period or throughout life were injected with PhIP (marked P). The experimental groups are as explained in the legend to Figure 1. n = 44–65. aSignificantly different from the negative control group given a 10% fat diet throughout life. bSignificantly different from the group given a 45% fat diet throughout life. cSignificantly different from the group given a 45% fat diet in utero and during nursing. dSignificantly different with PhIP compared with no PhIP exposure in the groups given a 45% fat diet during in utero and nursing period. eSignificantly different with PhIP compared with no PhIP exposure in the groups given a 45% fat diet throughout life. n.s. = not significantly different.
© Copyright Policy - open-access
Related In: Results  -  Collection

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fig9: The number of small intestinal tumors for pooled male and female Min/+ mice (mean ± SD). Two separate experimental groups receiving a 45% fat diet during in utero and nursing period or throughout life were injected with PhIP (marked P). The experimental groups are as explained in the legend to Figure 1. n = 44–65. aSignificantly different from the negative control group given a 10% fat diet throughout life. bSignificantly different from the group given a 45% fat diet throughout life. cSignificantly different from the group given a 45% fat diet in utero and during nursing. dSignificantly different with PhIP compared with no PhIP exposure in the groups given a 45% fat diet during in utero and nursing period. eSignificantly different with PhIP compared with no PhIP exposure in the groups given a 45% fat diet throughout life. n.s. = not significantly different.
Mentions: All mice had small intestinal tumors (adenomas), independent of dietary or carcinogenic exposures, confirming 100% incidence of small intestinal tumors as is commonly found in the Min/+ mice [25–27, 33]. The number of small intestinal tumors was not significantly different between the genders, thus the data for males and females are presented together (Figure 9). Although slightly increased, exposure to the 45% fat diet only in utero did not significantly increase the number of small intestinal tumors compared with the negative control group given a 10% fat diet throughout life. Exposure to a 45% fat diet only during the nursing period was significantly increased compared with the negative control group (P < 0.05). However, exposure to a 45% fat diet both in utero and during nursing, significantly increased the number of small intestinal tumors further, compared with the negative control group (P < 0.05), and compared with a 45% diet only in utero (P < 0.05), but not compared with only during nursing. Thus the effect of a 45% fat diet during the nursing period is more efficient in increasing the tumor number than the exposure in utero.

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