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Effect of Food Restriction and Leptin Supplementation on Fetal Programming in Mice

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Effect of Food Restriction and Leptin Supplementation on Fetal Programming in Mice REPRODUCTION-DEVELOPMENT Effect of Food Restriction and Leptin Supplementation on Fetal Programming in Mice Kathleen A. Pennington, Jennifer L. Harper, Ashley N. Sigafoos, Lindsey M. Beffa, Stephanie M. Carleton, Charlotte L. Phillips, and Laura C. Schulz Division of Reproductive and Perinatal Research (K.A.P., J.L.H., A.N.S., L.M.B., L.C.S.), Departments of Obstetrics, Gynecology, and Women’s Health, University of Missouri, Columbia, Missouri 65212; and Downloaded from https://academic.oup.com/endo/article/153/9/4556/2424252 by guest on 29 September 2021 Department of Biochemistry (S.M.C., C.L.P.), University of Missouri, Columbia, Missouri 65212 Metabolic disease is a significant global health and economic problem. In a phenomenon referred to as fetal programming, offspring of underweight or overweight mothers have an increased incidence of adulthood obesity and metabolic disease. Undernourished individuals have decreased levels of leptin, a regulator of energy balance, whereas obese people develop hyperleptinemia and leptin resistance. We hypothesize that alterations in circulating leptin during pregnancy contribute to programming events caused by maternal nutritional status. To test this hypothesis, pregnant mice were randomly placed in one of three treatment groups: ad libitum feed plus saline injection (control, n ϭ 5), 50% food restriction plus saline injection (restricted, n ϭ 4), or 50% food restriction plus 1 mg/kg⅐d leptin injection (restricted, leptin treated, n ϭ 4). Mice were treated from 1.5 to 11.5 d after conception and then returned to ad libitum feeding until weaning. At 19 wk after weaning, offspring were placed on a 45% fat diet and then followed up until 26 wk after weaning, at which time they were killed, and samples were collected for further analysis. Our results dem- onstrate that males are more negatively impacted by high-fat diet than females, regardless of maternal treatment. We provide evidence that differential response to leptin may mediate the sexual dimorphism observed in fetal programming in which male offspring are more affected by maternal undernutrition and female offspring by maternal overnutrition. We show that female offspring born to food-restricted, leptin-supplemented mothers are obese and insulin resistant. This may mimic fetal programming events seen in offspring of overweight women. (Endocrinology 153: 4556–4567, 2012) besity and its associated diseases are a significant into adulthood, which can include increased risk of met- Oproblem worldwide, having major effects on mor- abolic syndrome (2, 4). This hypothesis was put forth by bidity and mortality rates (1). The World Health Organi- epidemiologists Barker and Osmond (5), who discovered zation in 2005 predicted that by 2010 in the United States, correlations between adult cardiovascular disease and low 44.2% of adult males and 48.3% of adult females would birth weight, infant mortality, and poor maternal health, be obese [body mass index (BMI) Ն 30 kg/m2] (1). A study and nutrition. in 2010 estimated that 34.3–38.5% of all adults suffer Both maternal undernutrition and overnutrition are as- from metabolic syndrome, a condition characterized by sociated with fetal programming events, although the pre- central obesity, diabetes, hypertension, and nonalcoholic ponderance of data suggests that male offspring are more fatty liver disease (NAFLD), which accounts for 6–7% of influenced by the former and female offspring by the latter all mortalities (2, 3). The developmental origins of health (6–11). Studies from the Dutch Hunger Winter indicated and disease, or fetal programming, hypothesis states that that men born to mothers who were undernourished early the maternal environment has lasting effects on the fetus in pregnancy have a higher incidence of cardiovascular ISSN Print 0013-7227 ISSN Online 1945-7170 Abbreviations: BMI, Body mass index; ␮CT, microcomputed tomography; dpc, d after Printed in U.S.A. conception; GLM, general linear model; HFD, high-fat diet; IPGTT, ip glucose tolerance test; Copyright © 2012 by The Endocrine Society MRI, magnetic resonance imaging; NAFLD, nonalcoholic fatty liver disease; PFA, doi: 10.1210/en.2012-1119 Received January 30, 2012. Accepted June 20, 2012. paraformaldehyde. First Published Online July 9, 2012 4556 endo.endojournals.org Endocrinology, September 2012, 153(9):4556–4567 Endocrinology, September 2012, 153(9):4556–4567 endo.endojournals.org 4557 disease and obesity in middle age (7) compared with their Materials and Methods counterparts. In these studies, women were largely not Animals and tissue collection followed up due to tracking difficulties. However, when All animal procedures were approved by University of Mis- the phenomenon was replicated in animal models, includ- souri Institutional Animal Care and Use Committee and per- ing rats and sheep, maternal undernutrition during early formed in accordance with the National Institutes of Health pregnancy often programmed greater adverse outcomes in Guide for the Care and Use of Laboratory Animals. male offspring (6, 8, 12–15), although a few studies in Swiss-Webster female mice (Harlan, Indianapolis, IN) aged sheep show a negative effect of early pregnancy food re- 13–17 wk, were individually housed, and daily food consump- striction on female offspring (16, 17). On the other hand, tion was measured for 2 wk before mating as previously de- scribed (31). Mice were mated and then randomly placed in one global maternal nutrient restriction throughout preg- Downloaded from https://academic.oup.com/endo/article/153/9/4556/2424252 by guest on 29 September 2021 of three treatment groups: ad libitum feed plus saline injection nancy results in multiple aspects of metabolic syndrome in (control, n ϭ 5), 50% food restriction plus saline injection (re- both male and female offspring (18–20). In maternal over stricted, n ϭ 8), or 50% food restricted plus 1 mg/kg ⅐ d ip leptin nutrition studies, some studies indicate maternal obesity injection (restricted, leptin treated, n ϭ 8). Mice were placed on can have a negative impact on both sexes (21–24), whereas treatment at 1.5 d after conception (dpc) for 10 d, with injections other studies show a greater, or exclusive, negative impact at 1400 h and food introduced at 1600 h. After treatment, mice were returned to ad libitum feeding. Litter size was recorded and on female offspring born to overweight mothers, resulting then reduced to eight by culling randomly selected pups to con- in obesity, hypertension, and diabetes (9–11). However, trol for litter size during lactation. The sex ratio was determined no studies that have examined both sexes have shown either by visualization at weaning or by PCR for sex determining greater impact of maternal obesity on male offspring. region Y on tail clip DNA taken at culling, as previously de- Taken together these studies highlight the differences and scribed (32). Litters were weighed weekly until weaning at 3 wk similarities between maternal under- and overnutrition as of age. At weaning, pups were group housed by sex and treat- ment with up to four males or five females per cage and indi- well as the critical role timing and offspring sex have on the vidually weighed weekly. At 22 wk of age, all offspring were outcomes of fetal programming. placed on a 45% fat diet (Research Diets, New Brunswick, NJ) One key hormonal regulator of nutritional status and until the animals were killed. Ad libitum-fed offspring were energy homeostasis is leptin (25, 26). Circulating leptin killed by carbon dioxide inhalation at 29 wk of age for tissue levels are positively correlated to BMI (27), with hyper- collection. leptinemia and leptin resistance occurring in obesity (25). Blood samples were taken from all offspring at the time the animals were killed, and serum was stored at Ϫ20 C. Liver sam- In addition to its role in energy homeostasis, leptin affects ples were collected and placed in trireagent (Sigma, St. Louis, development in tissues including placenta, hypothalamus, MO) or fixed in 4% paraformaldehyde (PFA) overnight and then bone (28), and muscle (29). Furthermore, postnatal leptin embedded in optimum cutting temperature compound (Fisher levels influence the programming of adult disease (see the Scientific, Pittsburgh, PA) and stored at Ϫ80 C. Subcutaneous review in Ref. 30). Thus, we hypothesize that alterations fat, visceral fat, and hypothalamus samples were snap frozen in liquid nitrogen. All samples were stored at Ϫ80 C. The left kid- in circulating leptin levels during pregnancy contribute to ney was collected, fixed in 4% PFA, bisected midsagitally, em- fetal programming events caused by changes in maternal bedded in paraffin, and stored at room temperature. A sample of nutritional status. To test this, we have replicated the pancreas was also collected, fixed in 4% PFA, embedded in par- model of early pregnancy caloric restriction (7, 12) by affin, and stored at room temperature. Femurs were collected, feeding mice 50% of ad libitum consumption levels from cleaned, wrapped in gauze, and stored at Ϫ20 C in PBS. d 1.5 to 11.5 of pregnancy, a regimen that, as we previ- ously demonstrated, severely reduces serum leptin con- Small animal magnetic resonance imaging (MRI) Body composition was determined in 54 male offspring at 21 centrations (31). A subset of the food-restricted mice were wk of age and 54 male and 44 female offspring at 27 wk of age given daily leptin injections. We predicted that offspring after 5 wk exposure to a high-fat diet (HFD). Body fat percentage programming would be related to maternal hyper- or hy- was measured using a Micro-MRI high performance 7T MR poleptinemia, not to nutrient status per se. In other words, imaging and spectroscopy system (Varian Inc., Santa Clara, CA) metabolic programming would be evident in male off- at the Veterans Affairs Biomolecular Imaging Center at the spring of nutrient-restricted mothers but not when restric- Harry S. Truman Veterans Affairs Hospital and University of Missouri-Columbia, as previously described (33).
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