The effects of prenatal exposure to a ‘junk food’ diet on offspring food preferences and fat deposition can be mitigated by improved nutrition during lactation

Exposure to a maternal junk food (JF) diet in utero and during the suckling period has been demonstrated to increase the preference for palatable food and increase the susceptibility to diet-induced obesity in adult offspring. We aimed to determine whether the effects of prenatal exposure to JF could be ameliorated by cross-fostering offspring onto dams consuming a standard rodent chow during the suckling period. We report here that when all offspring were given free access to the JF diet for 7 weeks from 10 weeks of age, male offspring of control (C) or JF dams that were cross-fostered at birth onto JF dams (C-JF, JF-JF), exhibited higher fat (C-C: 12.3 ± 0.34 g/kg/day; C-JF: 14.7 ± 1.04 g/kg/day; JF-C: 11.5 ± 0.41 g/kg/day; JF-JF: 14.0 ± 0.44 g/kg/day; P < 0.05) and overall energy intake (C-C: 930.1 ± 18.56 kJ/kg/day; C-JF: 1029.0 ± 82.9 kJ/kg/day; JF-C: 878.3 ± 19.5 kJ/kg/day; JF-JF: 1003.4 ± 25.97 kJ/kg/day; P < 0.05) than offspring exposed to the JF diet only before birth (JF-C) or not at all (C-C). Female offspring suckled by JF dams, despite no differences in food intake, had increased fat mass as percentage of body weight (C-C: 19.9 ± 1.33%; C-JF: 22.8 ± 1.57%; JF-C: 17.4 ± 1.03%; JF-JF: 22.0 ± 1.0%; P < 0.05) after 3 weeks on the JF diet. No difference in fat mass was observed in male offspring. These findings suggest that the effects of prenatal exposure to a JF diet on food preferences in females and susceptibility to diet-induced obesity in males can be prevented by improved nutrition during the suckling period.

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Maternal Junk Food Diets: The Effects on Offspring Fat Mass and Food Preferences

Diet, Nutrition, and Fetal Programming ◽

10.1007/978-3-319-60289-9_18 ◽

2017 ◽

pp. 227-238 ◽

Cited By ~ 2

Author(s):

Beverly S. Muhlhausler ◽

Jessica R. Gugusheff ◽

Simon C. Langley-Evans

Keyword(s):

Fat Mass ◽

Food Preferences ◽

Junk Food

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Consuming a low-fat diet from weaning to adulthood reverses the programming of food preferences in male, but not in female, offspring of ‘junk food’-fed rat dams

Acta Physiologica ◽

10.1111/apha.12132 ◽

2013 ◽

Vol 210 (1) ◽

pp. 127-141 ◽

Cited By ~ 19

Author(s):

Z. Y. Ong ◽

B. S. Muhlhausler

Keyword(s):

Food Preferences ◽

Female Offspring ◽

Junk Food ◽

Low Fat ◽

Low Fat Diet

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Sex differences in prenatal programming of hypertension by dexamethasone

Experimental Biology and Medicine ◽

10.1177/15353702211003294 ◽

2021 ◽

pp. 153537022110032

Author(s):

Issa Alhamoud ◽

Susan K Legan ◽

Jyothsna Gattineni ◽

Michel Baum

Keyword(s):

Blood Pressure ◽

Plasma Renin ◽

Female Offspring ◽

Male Offspring ◽

Thick Ascending Limb ◽

Protein Abundance ◽

Female Rat ◽

Prenatal Programming ◽

Transporter Protein ◽

Renal Tubular

Prenatal dexamethasone has been shown to increase blood pressure in male offspring but the mechanism for the increase in blood pressure is unclear. The present study examined if prenatal programming by maternal injection of dexamethasone on days 15 and 16 of gestation affected the blood pressure comparably in female and male offspring. Our hypothesis was that males would be affected by prenatal dexamethasone to a greater extent than females and that either an increase in renal tubular transporter abundance or an increase in renin or aldosterone system would be associated with hypertension with prenatal programming. Prenatal dexamethasone increased blood pressure at two months and six months of age and resulted in proteinuria and albuminuria at six months in male but not female rat offspring. There was no effect of prenatal dexamethasone on blood pressure and proteinuria at one month in male and in female offspring. While prenatal dexamethasone increased male renal thick ascending limb sodium potassium two chloride cotransporter protein abundance at two months, prenatal dexamethasone on days 15 and 16 of gestation did not affect transporter abundance in males at other ages, nor did it affect proximal tubule sodium/hydrogen exchanger or distal convoluted tubule sodium chloride cotransporter protein abundance at any age. There was no difference in systemic renin or aldosterone in the prenatal dexamethasone group compared to same sex controls. In conclusion, male but not female offspring have an increase in blood pressure and urinary protein excretion with prenatal dexamethasone. The increase in blood pressure with prenatal programming was not associated with a consistent increase in renal tubular transporter protein abundance, nor plasma renin activity and serum aldosterone.

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PERFORMANCE OF DWARF BROILER BREEDERS IN LAYING CAGES AND FLOOR PENS AND OF NORMAL BREEDERS IN FLOOR PENS

Canadian Journal of Animal Science ◽

10.4141/cjas75-089 ◽

1975 ◽

Vol 55 (4) ◽

pp. 741-747 ◽

Cited By ~ 3

Author(s):

J. H. STRAIN ◽

A. P. PILOSKI

Keyword(s):

Body Weight ◽

Egg Production ◽

General Pattern ◽

Female Offspring ◽

Male Offspring ◽

Production Cycle ◽

Feed Conversion ◽

Broiler Breeders ◽

Feed Costs

Dwarf broiler breeders in single-bird cages (DC), in floor pens (DF) and normal broiler breeders in floor pens (NF) were compared for their own and their offspring’s performance. No differences were observed in rate of egg production at 147–329 days of age between the NF and DF birds (48 vs. 47%) whereas the DC birds laid at the rate of 40%. Hen-housed egg numbers for the same period followed the same general pattern (NF, 81; DF, 82; DC, 70 eggs/bird). DF and DC birds consumed less feed per dozen eggs than the NF birds (3.4 vs. 4.3 kg/doz). Egg weights in the early part of the production cycle were not significantly different among the groups but at 294 days of age the normal birds laid larger eggs than the dwarfs (65 vs. 62 g). Dwarfs in cages reached 50% production earlier than the DF or NF birds. Female offspring from the three groups grew at the same rate and weighed 1.7 kg at 56 days of age but there were significant differences in feed conversion (NF, 2.46; DF, 2.43; DC, 2.53 kg/kg body weight produced). Male offspring had small but not statistically significant differences in body weight at 56 days (NF, 2.16; DF, 2.12; DC, 2.09 kg) or feed conversion (NF, 2.30; DF, 2.29; DC, 2.34 kg/kg body weight). Mortality in the offspring ranged from 2.7 to 9.2% but did not differ significantly. Income over feed costs per broiler started did not differ from the three groups regardless of the meat price – feed price combination considered. However, when profit was computed on a breeder hen basis, the DF females were more profitable than either the NF or DC females.

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Dietary Isoliquiritigenin at a Low Dose Ameliorates Insulin Resistance and NAFLD in Diet-Induced Obesity in C57BL/6J Mice

International Journal of Molecular Sciences ◽

10.3390/ijms19103281 ◽

2018 ◽

Vol 19 (10) ◽

pp. 3281 ◽

Cited By ~ 4

Author(s):

Youngmi Lee ◽

Eun-Young Kwon ◽

Myung-Sook Choi

Keyword(s):

Insulin Resistance ◽

Energy Expenditure ◽

Body Fat ◽

Fat Mass ◽

High Fat Diet ◽

Plasma Cholesterol ◽

Cellular Respiration ◽

Body Fat Mass ◽

High Fat ◽

Diet Induced Obesity

Isoliquiritigenin (ILG) is a flavonoid constituent of Glycyrrhizae plants. The current study investigated the effects of ILG on diet-induced obesity and metabolic diseases. C57BL/6J mice were fed a normal diet (AIN-76 purified diet), high-fat diet (40 kcal% fat), and high-fat diet +0.02% (w/w) ILG for 16 weeks. Supplementation of ILG resulted in decreased body fat mass and plasma cholesterol level. ILG ameliorated hepatic steatosis by suppressing the expression of hepatic lipogenesis genes and hepatic triglyceride and fatty acid contents, while enhancing β-oxidation in the liver. ILG improved insulin resistance by lowering plasma glucose and insulin levels. This was also demonstrated by the intraperitoneal glucose tolerance test (IPGTT). Additionally, ILG upregulated the expression of insulin signaling-related genes in the liver and muscle. Interestingly, ILG elevated energy expenditure by increasing the expression of thermogenesis genes, which is linked to stimulated mitochondrial biogenesis and uncoupled cellular respiration in brown adipose tissue. ILG also suppressed proinflammatory cytokine levels in the plasma. These results suggest that ILG supplemented at 0.02% in the diet can ameliorate body fat mass, plasma cholesterol, non-alcoholic fatty liver disease, and insulin resistance; these effects were partly mediated by increasing energy expenditure in high-fat fed mice.

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High Dietary Fat Intake during Lactation Promotes Development of Diet-Induced Obesity in Male Offspring of Mice

Journal of Nutritional Science and Vitaminology ◽

10.3177/jnsv.59.384 ◽

2013 ◽

Vol 59 (5) ◽

pp. 384-392 ◽

Cited By ~ 19

Author(s):

Tsuyoshi TSUDUKI ◽

Yasuna KITANO ◽

Taro HONMA ◽

Ryo KIJIMA ◽

Ikuo IKEDA

Keyword(s):

Dietary Fat ◽

Male Offspring ◽

Fat Intake ◽

Dietary Fat Intake ◽

Diet Induced Obesity

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Maternal high fat feeding results in higher fat mass and bone mineral content in weanling but not 3 month old female offspring

The FASEB Journal ◽

10.1096/fasebj.27.1_supplement.244.7 ◽

2013 ◽

Vol 27 (S1) ◽

Author(s):

Laura M Castelli ◽

Paula M Miotto ◽

Rebecca EK MacPherson ◽

Bryan D Johnston ◽

Paul J LeBlanc ◽

...

Keyword(s):

Bone Mineral Content ◽

Bone Mineral ◽

Fat Mass ◽

Mineral Content ◽

Female Offspring ◽

High Fat ◽

Fat Feeding

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Carbonyl Reductase 1 Overexpression in Adipose Amplifies Local Glucocorticoid Action and Impairs Glucose Tolerance in Lean Mice

Journal of the Endocrine Society ◽

10.1210/jendso/bvab048.1639 ◽

2021 ◽

Vol 5 (Supplement_1) ◽

pp. A806-A806

Author(s):

Rachel Bell ◽

Elisa Villalobos ◽

Mark Nixon ◽

Allende Miguelez-Crespo ◽

Matthew Sharp ◽

...

Keyword(s):

Adipose Tissue ◽

Glucose Tolerance ◽

Fat Mass ◽

High Fat Diet ◽

Fasting Glucose ◽

High Fat ◽

Male And Female ◽

Over Expression ◽

Female Mice ◽

Diet Induced Obesity

Abstract Glucocorticoids play a critical role in metabolic homeostasis. Chronic or excessive activation of the glucocorticoid receptor (GR) in adipose tissue contributes to metabolic disorders such as glucose intolerance and insulin resistance. Steroid-metabolising enzymes in adipose, such as 11β-HSD1 or 5α-reductase, modulate the activation of GR by converting primary glucocorticoids into more or less potent ligands. Carbonyl reductase 1 (CBR1) is a novel regulator of glucocorticoid metabolism, converting corticosterone/cortisol to 20β-dihydrocorticosterone/cortisol (20β-DHB/F); a metabolite which retains GR activity. CBR1 is abundant in adipose tissue and increased in obese adipose of mice and humans1 and increased Cbr1 expression is associated with increased fasting glucose1. We hypothesised that increased Cbr1/20β-DHB in obese adipose contributes to excessive GR activation and worsens glucose tolerance. We generated a novel murine model of adipose-specific Cbr1 over-expression (R26-Cbr1Adpq) by crossing conditional knock-in mice with Adiponectin-Cre mice. CBR1 protein and activity were doubled in subcutaneous adipose tissue of male and female R26-Cbr1Adpq mice compared with floxed controls; corresponding to a two-fold increase 20β-DHB (1.6 vs. 4.2ng/g adipose; P=0.0003; n=5-7/group). There were no differences in plasma 20β-DHB or corticosterone. Bodyweight, lean or fat mass, did not differ between male or female R26-Cbr1Adpq mice and floxed controls. Lean male R26-Cbr1Adpq mice had higher fasting glucose (9.5±0.3 vs. 8.4±0.3mmol/L; P=0.04) and worsened glucose tolerance (AUC 1819±66 vs. 1392±14; P=0.03). Female R26-Cbr1Adpq mice also had a worsened glucose tolerance but fasting glucose was not altered with genotype. There were no differences in fasting insulin or non-esterified fatty acid between genotypes in either sex. Expression of GR-induced genes Pnpla2, Gilz and Per1, were increased in adipose of R26-Cbr1Adpq mice. Following high-fat diet induced obesity, no differences in bodyweight, lean or fat mass, with genotype were observed in male and female mice, and genotype differences in fasting glucose and glucose tolerance were abolished. In conclusion, adipose-specific over-expression of Cbr1 in lean male and female mice led to increased levels of 20β-DHB in adipose but not plasma, and both sexes having worsened glucose tolerance. The influence of adipose CBR1/20β-DHB on glucose tolerance was not associated with altered fat mass or bodyweight and was attenuated by high-fat diet-induced obesity. These metabolic consequences of Cbr1 manipulation require careful consideration given the wide variation in CBR1 expression in the human population, the presence of inhibitors and enhancers in many foodstuffs and the proposed use of inhibitors as an adjunct for cancer treatment regimens. Reference: Morgan et al., Scientific Reports. 2017; 7.

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Prevention of diet-induced obesity and impaired glucose tolerance in rats following administration of leptin to their mothers

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00676.2006 ◽

2007 ◽

Vol 292 (5) ◽

pp. R1810-R1818 ◽

Cited By ~ 49

Author(s):

Claire J. Stocker ◽

Ed Wargent ◽

Jacqueline O'Dowd ◽

Claire Cornick ◽

John R. Speakman ◽

...

Keyword(s):

Weight Gain ◽

Energy Balance ◽

Glucose Tolerance ◽

Female Offspring ◽

Male Offspring ◽

Male Rats ◽

Fat Pad ◽

Plasma Insulin Concentration ◽

Obesogenic Diet ◽

Tolerance Curve

Absence of leptin is known to disrupt the development of energy balance regulatory mechanisms. We investigated whether administration of leptin to normally nourished rats affects energy balance in their offspring. Leptin (2 mg·kg−1·day−1) was administered from day 14 of pregnancy and throughout lactation. Male and female offspring were fed either on chow or on high-fat diets that elicited similar levels of obesity in the sexes from 6 wk to 15 mo of age. Treatment of the dams with leptin prevented diet-induced increases in the rate of weight gain, retroperitoneal fat pad weight, area under the intraperitoneal glucose tolerance curve, and fasting plasma insulin concentration in female offspring. In the male offspring, the diet-induced increase in weight gain was prevented and increased fat pad weight was reduced. Energy intake per rat was higher in response to the obesogenic diet in male offspring of saline-treated but not leptin-treated dams. A similar trend was seen in 3-mo-old female offspring. Energy expenditure at 3 mo of age was higher for a given body weight in female offspring of leptin-treated compared with saline-treated dams when these animals were fed on the obesogenic diet. A similar trend was seen for male rats fed on the obesogenic diet. Thus leptin levels during pregnancy and lactation can affect the development of energy balance regulatory systems in their offspring.

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