A maternal 'junk food' diet in pregnancy and lactation promotes an exacerbated taste for 'junk food' and a greater propensity for obesity in rat offspring

Obesity is generally associated with high intake of junk foods rich in energy, fat, sugar and salt combined with a dysfunctional control of appetite and lack of exercise. There is some evidence to suggest that appetite and body mass can be influenced by maternal food intake during the fetal and suckling life of an individual. However, the influence of a maternal junk food diet during pregnancy and lactation on the feeding behaviour and weight gain of the offspring remains largely uncharacterised. In this study, six groups of rats were fed either rodent chow alone or with a junk food diet during gestation, lactation and/or post-weaning. The daily food intakes and body mass were measured in forty-two pregnant and lactating mothers as well as in 216 offspring from weaning up to 10 weeks of age. Results showed that 10 week-old rats born to mothers fed the junk food diet during gestation and lactation developed an exacerbated preference for fatty, sugary and salty foods at the expense of protein-rich foods when compared with offspring fed a balanced chow diet prior to weaning or during lactation alone. Male and female offspring exposed to the junk food diet throughout the study also exhibited increased body weight and BMI compared with all other offspring. This study shows that a maternal junk food diet during pregnancy and lactation may be an important contributing factor in the development of obesity.     

Early exposure of dams to a westernized diet has long-term consequences on food intake and physiometabolic homeostasis of the rat offspring

This study evaluated the long-term effects of a westernized diet during pregnancy and lactation. Female Wistar rats (n?=?12) were divided into two groups according to their food intake, namely, control (C) or westernized (W) diet, throughout pregnancy/lactation. On the 21st day, the male pups were weaned on a standard diet as follows: Control diet (CC) (n?=?8) and westernized diet in perinatal life followed by control diet post weaning (WC) (n?=?8). The levels of fasting (12?h) serum glucose, triglycerides (TG), and total cholesterol and fraction in the pups were determined. During weaning, the WC group showed 14% greater body weight (p?相似文献   

Glucose intolerance associated with early-life exposure to maternal cafeteria feeding is dependent upon post-weaning diet

In addition to being a risk factor for adverse outcomes of pregnancy, maternal obesity may play a role in determining the long-term disease patterns observed in the resulting offspring, with metabolic and dietary factors directly programming fetal development. The present study evaluated the potential for feeding rats an obesogenic cafeteria diet (O) pre-pregnancy, during pregnancy, during lactation and for the offspring post-weaning, to programme glucose tolerance. Early-life exposure to an O diet had no significant effect on offspring food intake. Early-life programming associated with O feeding to induce maternal obesity was associated with reduced adiposity in offspring weaned onto low-fat chow. Adult offspring exposed to an O diet in early life and weaned on a chow diet had low fasting glucose and insulin concentrations and appeared to be more sensitive to insulin during an intraperitoneal glucose tolerance test. When weaned on an O diet, male offspring were more prone to glucose intolerance than females. On the basis of the area under the glucose curve, maternal O feeding at any point from pre-mating to lactation was associated with impaired glucose tolerance. The mechanism for this was not identified, although increased hepatic expression of Akt2 may have indicated disturbance of insulin signalling pathways. The observations in the present study confirm that maternal overnutrition and obesity during pregnancy are risk factors for metabolic disturbance in the resulting offspring. Although the effects on glucose homeostasis were independent of offspring adiposity, the programming of a glucose-intolerant phenotype was only observed when offspring were weaned on a diet that induced greater fat deposition.     

Low intensity exercise and varying proportions of dietary glucose and fat modify milk and mammary gland compositions and pup growth.

Exercise during pregnancy or lactation may create a competition for glucose between the exercising muscle and either the developing fetus or the lactating mammary gland. To test these two hypotheses, pregnant rats were randomly assigned to isoenergetic diets with varying levels of glucose (20, 40 or 60% by weight) and fat (30, 22 or 14%, respectively, by weight) and were rested (R) or exercised (E) on a motorized treadmill at 20 m/min, 60 min/d (low intensity), 7 d/wk throughout pregnancy and lactation. Main effects and selected interactions of diet and exercise during pregnancy and diet, exercise and litter size during lactation were tested using 3 x 2 and 3 x 2 x 2 factorial designs, respectively. Neither diet nor exercise affected pregnancy outcomes. In contrast, during lactation, milk and mammary gland compositions and pup growth were altered. Exercise produced higher milk protein concentrations (40% glucose diet) and lower milk lactose concentrations (20% glucose diet). Exercise also lowered mammary gland fat content and produced higher milk fat concentrations. The 60% glucose diet resulted in the highest milk fat concentrations, but pups of dams fed the 40% diet were heavier on lactation d 15 than pups of dams fed the 60% diet. Taken together, these results support the claim of decreased availability of glucose to the mammary gland for lactose synthesis during chronic low intensity exercise. Additionally, the best lactation performance was not supported by a high carbohydrate (60% glucose), lower fat (14%) intake. A more moderate carbohydrate (40% glucose), higher fat (22%) intake promoted greater pup weights at weaning, suggesting an overlooked role for macronutrient composition in optimizing lactation performance.     

Effect of varying dietary zinc intake of weanling mouse pups during recovery from early undernutrition on growth, body composition and composition of gain

Catch-up growth during recovery from undernutrition is characterized by rapid body weight gain often marked by disproportionately high fat gain. In this study dietary zinc intake of mouse pups during recovery from undernutrition affected composition of gain as well as growth. Mouse pups were undernourished during the suckling period and then fed 25% casein recovery diets containing 5, 10, 40 or 110 micrograms Zn/g diet. Pups given dietary zinc levels of 40 micrograms Zn/g ad libitum achieved recovery body weights and had normal body composition. However, previously undernourished pups given marginal levels of dietary zinc (10 micrograms Zn/g diet) had similar food intakes, similar final body weights, lower lean body mass gains and greater fat gains (males only) than controls. Pups fed low zinc diets (5 micrograms Zn/g diet) were unable to attain recovery body weight and had less protein gain than previously undernourished animals fed higher zinc-containing diets or healthy pups fed the same zinc levels. The results were consistently more pronounced in males. Thus dietary zinc deficiency during catch-up growth after undernutrition limited both recovery and protein gain, whereas marginal dietary zinc intake limited protein gain in mice.     

Nutritional recovery with a soybean flour diet improves the insulin response to a glucose load without modifying glucose homeostasis

OBJECTIVE: We investigated the effect of nutritional recovery with a soybean flour diet on glucose tolerance, insulin response to a glucose load, and the action of insulin in adult rats exposed to a protein deficiency during intrauterine life and lactation. METHODS: Male Wistar rats from dams fed a normal- or low-protein diet during pregnancy and lactation were maintained after weaning by feeding them normal-protein isoenergetic diets containing soybean flour or casein and low-protein casein diet. RESULTS: Rats fed a soybean flour diet had a lower final body weight, epididymal fat pad, carcass fat content, and liver glycogen level. The serum glucose concentrations in the basal and fed states and the area under the glucose curves during the glucose tolerance test were not significantly different among the four groups. Their serum insulin levels during fasting were observed to be similar to those fed a casein diet. These rats also had a higher serum insulin levels in a fed state and total area under the insulin curves in response to a glucose load, but a lower ratio of area under the glucose/insulin curves during the glucose tolerance test than those fed a casein diet. CONCLUSION: These results indicate that nutritional recovery with a soybean flour diet improved the insulin response to a glucose load and decreased the sensitivity to insulin, at least in hepatic tissue.     

Maternal low-protein diet during lactation programmes body composition and glucose homeostasis in the adult rat offspring

Previously we have reported that maternal malnutrition during lactation programmes body weight and thyroid function in the adult offspring. In the present study we evaluated the effect of maternal protein restriction during lactation upon body composition and hormones related to glucose homeostasis in adult rats. During lactation, Wistar lactating rats and their pups were divided into two experimental groups: control (fed a normal diet; 23% protein) and protein-restricted (PR; fed a diet containing 8% protein). At weaning, offspring received a normal diet until they were 180 d old. Body weight (BW) and food intake were monitored. Serum, adrenal glands, visceral fat mass (VFM) and carcasses were collected. PR rats showed lower BW (-13%; P < 0.05), VFM (-33%; P < 0.05), total body fat (-33%; P < 0.05), serum glucose (-7%; P < 0.05), serum insulin (-26%, P < 0.05), homeostasis model assessment index (-20%), but higher total adrenal catecholamine content (+90%; P < 0.05) and serum corticosterone concentration (+51%; P < 0.05). No change was observed in food intake, protein mass or total body water. The lower BW of PR rats is due to a reduction of white fat tissue, probably caused by an increase in lipolysis or impairment of lipogenesis; both effects could be related to higher catecholaminergic status, as well as to hypoinsulinaemia. To conclude, changes in key hormones which control intermediary metabolism are programmed by maternal protein restriction during lactation, resulting in BW alterations in adult rats.     

Does perinatal omega-3 polyunsaturated fatty acid deficiency increase appetite signaling?

OBJECTIVE: To investigate the effect of maternal dietary omega-3 polyunsaturated fatty acid (PUFA) deficiency and repletion on food appetite signaling. RESEARCH METHODS AND PROCEDURES: Sprague-Dawley rat dams were maintained on diets either supplemented with (CON) or deficient in (DEF) omega-3 PUFA. All offspring were raised on the maternal diet until weaning. After weaning, two groups remained on the respective maternal diet (CON and DEF groups), whereas a third group, born of dams fed the DEF diet, were switched to the CON diet (REC). Experiments on food intake began when the male rats reached 16 weeks of age. Food intake was stimulated either by a period of food restriction, by blocking glucose utilization (by 2-deoxyglucose injection), or by blocking beta-oxidation of fatty acids (by beta-mercaptoacetate injection). RESULTS: DEF animals consumed more than CON animals in response to all stimuli, with the greatest difference (1.9-fold) demonstrated following administration of 2-deoxyglucose. REC animals also consumed more than CON animals in response to food restriction and 2-deoxyglucose but not to beta-mercaptoacetate. DISCUSSION: These findings indicate that supply of omega-3 PUFA, particularly during the perinatal period, plays a role in the normal development of mechanisms controlling food intake, especially glucoprivic (i.e. reduced glucose availability) appetite signaling. Dietary repletion of omega-3 PUFA from 3 weeks of age restored intake responses to fatty acid metabolite signaling but did not reverse those in response to food restriction or glucoprivic stimuli.     

Long-chain omega-3 fatty acid supply in pregnancy and lactation

PURPOSE OF REVIEW: Long-chain omega-3 fatty acids are essential for the developing fetus. Docosahexaenoic acid, the most important omega-3 fatty acid, is an important component of neural and retinal membranes, and rapidly accumulates in the brain during gestation and the postnatal period. Positive associations have been shown between maternal intake of fish, seafood and omega-3 fatty acids during pregnancy and/or lactation and visual and cognitive development. RECENT FINDINGS: The review focuses on new findings by both observational and interventional studies on the influence of omega-3 fatty acids during pregnancy or lactation on gestation length and birth weight, preterm delivery, preeclampsia, maternal depression and infant visual function and neural development. SUMMARY: Omega-3 fatty acids have been associated with reduced risk of cardiovascular and other diseases. Observational and interventional studies indicate a significant association with prolonging gestation and reducing the risk of preterm delivery both in low-risk and in high-risk pregnancies. Further benefits have been suggested for intrauterine growth restriction, preeclampsia and postpartum depression, but the evidence is inconclusive. Higher maternal docosahexaenoic acid intake both in pregnancy and lactation is associated with positive infant neurodevelopmental outcomes. Women of reproductive age should achieve an average dietary docosahexaenoic acid intake of at least 200 mg/day.     

Glucose turnover rate in the lactating rat: effect of feeding a high fat diet

Feeding a high fat diet during lactation should reduce the competition for glucose utilization between the mammary gland and the other maternal tissues, because dietary fat is directly utilized for milk lipid synthesis. Glucose homeostasis was studied in nonlactating and lactating rats fed a high fat diet and compared with that in rats fed a high carbohydrate diet. In nonlactating rats fed a high fat diet, blood glucose concentration was slightly higher, whereas plasma insulin concentration was lower than in nonlactating rats fed a high carbohydrate diet. In the postabsorptive state, plasma free fatty acids and blood ketone bodies were not modified by the nature of the diet consumed. Glucose turnover rate and glucose metabolic clearance rate in the postabsorptive state in nonlactating rats fed a high carbohydrate diet were not different from those in rats fed a high fat diet [9.5 +/- 1.4 vs. 8.8 +/- 0.8 mg/(min X kg) and 8.9 +/- 1.2 vs. 7.9 +/- 0.7 mL/(min X kg)]. In lactating rats, blood glucose and ketone bodies, plasma insulin and free fatty acid concentrations were not affected in the postabsorptive state by the composition of the diet consumed. The glucose metabolic clearance rate in lactating rats fed the high carbohydrate diet was higher than that in nonlactating rats fed the same diet. However, the glucose metabolic clearance rate in lactating rats fed the high fat diet was not different from that in nonlactating rats fed the same diet.     

Comparison between omega-3 and omega-6 polyunsaturated fatty acid intakes as assessed by a food frequency questionnaire and erythrocyte membrane fatty acid composition in young children

OBJECTIVE: We conducted a dietary validation study in youth aged 1-11 years by comparing dietary intake of omega-3 and omega-6 polyunsaturated fatty acids (PUFAs) as assessed by a parent-completed semiquantitative food frequency questionnaire (FFQ) over time to erythrocyte membrane composition of the same fatty acids. DESIGN: The study population included youth aged 1-11 years who were participants in the Diabetes Autoimmunity Study in the Young (DAISY), a longitudinal study in Denver, Colorado that is following a cohort of youth at risk for developing type I diabetes. Four hundred and four children who had erythrocyte membrane fatty acid data matched to an FFQ corresponding to the same time frame for a total of 917 visits (matches) were included. PUFA intake was expressed both as g/day (adjusted for total energy) and as percent of total fat intake. We used mixed models to test the association and calculate the correlation between the erythrocyte membrane estimates and PUFA intake using all records of data for each youth. RESULTS: Intakes of total omega-3 fatty acids (beta=0.52, P<0.0001, rho=0.23) and marine PUFAs (beta=1.62, P<0.0001, rho=0.42), as a percent of total fat in the diet, were associated with percent of omega-3 and marine PUFAs in the erythrocyte membrane. Intakes of omega-6 PUFAs (beta=0.04, P=0.418, rho=0.05) and arachidonic acid (beta=0.31, P=0.774, rho=0.01) were not associated. CONCLUSIONS: In these young children, an FFQ using parental report provided estimates of average long-term intakes of marine PUFAs that correlated well with their erythrocyte cell membrane fatty acid status.     

Trans fatty acids in maternal milk lead to cardiac insulin resistance in adult offspring

OBJECTIVE: Trans fatty acids (TFAs) are derived from vegetable oil hydrogenation and can be found in most manufactured food products. Our main objective was to evaluate the effects of TFA consumption by lactating dams on cardiac glucose metabolism of adult offspring by analyzing glucose transporter-4 in the left ventricle. To investigate the energy homeostasis, insulin sensitivity and hepatic glycogen content were also measured. METHODS: Lactating Wistar rats were divided into a control group or a TFA group. The control group received a diet containing soybean oil, and the TFA group received a diet containing partially hydrogenated vegetable oil (total trans concentration of about 10.58 mg/g, 11.75%, of total fat) throughout the lactation period. At weaning, pups from both groups received a standard chow until 60 d of age, at which time the quantity of glucose transporter-4 in the left ventricle and hepatic glycogen were measured. Moreover, insulin sensitivity was analyzed by assessing the insulin/glucose ratio and the homeostatic model assessment index. RESULTS: TFA consumption by the pups during lactation led to a significant decrease in the cardiac content of glucose transporter-4 (P < 0.05) and in the hepatic content of glycogen (P < 0.05). Moreover, we observed impaired insulin sensitivity in the TFA group (insulin/glucose ratio and homeostatic model assessment index, P < 0.05) in adulthood. CONCLUSION: Our data suggest that the consumption of hydrogenated fat, rich in TFAs, by the mothers during the lactation period caused cardiac insulin resistance in the adult progeny, thus reinforcing the hypothesis that early adaptations may cause deleterious consequences later in life.     

Gender difference in the effect of intrauterine malnutrition on the central anorexigenic action of insulin in adult rats

OBJECTIVE: We evaluated whether insulin hypophagia and hypothalamic signaling are affected in adult rats exposed to intrauterine undernutrition. METHODS: Pregnant rats ate ad libitum throughout pregnancy and lactation (control, C) or 50% of control intake in the first 2 wk of pregnancy (restricted, R). Four-month-old C and R progeny received insulin or vehicle intracerebroventricular injections for evaluation of 24-h food intake, hypothalamic insulin receptor (IR), and IR substrate-1 (IRS-1) protein content and tyrosine phosphorylation, pp185 phosphorylation, and IRS-1 association with phosphatidylinositol 3-kinase (PI3-K). RESULTS: With respect to males, R males had normal body composition and insulin-induced hypophagia. IR protein levels were lower but IR phosphorylation was higher in R than in C males. IRS-1 levels and phosphorylation were similar between C and R males, insulin stimulated an IRS-1/PI3-K association in C but not in R males, and pp185 phosphorylation was higher in R than in C males. For females, body fat and serum leptin were elevated in R females. Insulin inhibited food intake in C but not in R females. Insulin-induced IR phosphorylation and protein levels of IR and IRS-1 were higher in R than in C females. However, IRS-1 and pp185 phosphorylation and IRS-1/PI3-K association were significantly stimulated by insulin in C but not in R females. CONCLUSIONS: Female adult rats exposed to intrauterine undernutrition had increased adiposity, marked impairment of hypothalamic insulin signaling, and loss of insulin-induced hypophagia. These disturbances were less severe or even absent in male progeny. The findings show that female progeny are more susceptible than their male siblings to the effects of maternal malnutrition.     

Soy protein-based compared with casein-based diets fed during pregnancy and lactation increase food intake and characteristics of metabolic syndrome less in female than male rat offspring

We hypothesized that soy protein (S)-based diets fed during pregnancy and lactation increase food intake and the presence of characteristics of the metabolic syndrome to a lesser extent in female than in male rats. Soy protein- and casein (C)-based American Institute of Nutrition-93G diets were fed to 2 groups (n = 12 per group) of pregnant Wistar rats from day 3 of gestation and throughout lactation. Their effects on characteristics of metabolic syndrome and food intake regulation in female pups maintained for 15 weeks on the C diet were compared. Body weight (BW) and food intake (FI) were measured weekly. Fat pad mass was measured at birth, at weaning, and at week 15. Glucose and insulin tolerance tests were conducted at weeks 8 and 12; and systolic and diastolic blood pressures were measured at weeks 4, 8, and 12. Plasma was collected at weaning and at the end of the studies for glucose, insulin, glucagon-like peptide 1, peptide YY, and ghrelin. Food intake in response to protein preloads was measured at week 7. Feeding the S diet throughout gestation and lactation resulted in higher systolic blood pressure (P < .005), FI (P < .05), and glucagon-like peptide 1 and lower peptide YY at weaning and higher BW during weeks 11 to 15 and fat pad mass at week 15 (all Ps < .05). However, no sign of insulin resistance was found; nor was short-term FI in response to protein preloads affected. In conclusion, S- compared with C-based American Institute of Nutrition-93 G diets consumed throughout gestation and lactation increased BW and FI later and resulted in fewer characteristics of metabolic syndrome in female than in male offspring.     

Intake of trans fatty acid-rich hydrogenated fat during pregnancy and lactation inhibits the hypophagic effect of central insulin in the adult offspring

OBJECTIVE: Using rats we examined whether maternal intake of hydrogenated fat rich in trans fatty acids affects brain fatty acid profile, hypothalamic content of insulin receptor and insulin receptor substrate-1 proteins, and the hypophagic effect of centrally administered insulin in 3-mo-old male progeny. METHODS: Throughout pregnancy and lactation, Wistar rats ate isocaloric/normolipidic diets with soybean oil (control) or soybean oil-derived hydrogenated fat (trans diet) as a fat source. Upon weaning, the trans offspring continued on the trans diet (trans group) or were switched to a control diet (trans-control group). RESULTS: Compared with control rats, trans rats had lower brain levels of eicosapentaenoic acid. Compared with trans rats, trans-control rats had increased levels of total polyunsaturated fatty acids and arachidonic acid and decreased levels of trans fatty acids, saturated fatty acids, and monounsaturated fatty acids. Insulin receptor and insulin receptor substrate-1 levels were significantly lower (44% and 38%, respectively) in trans than in control rats. In trans-control rats, insulin receptor was 26% lower (P < 0.05), whereas insulin receptor substrate-1 was 50% lower, than in control rats. Insulin decreased 24-h feeding in control (27%) and trans (38%) rats but failed to do so in trans-control rats. The latter group had increased serum glucose levels. CONCLUSIONS: The data suggest that the early (intrauterine/perinatal) exposure to hydrogenated fat rich in trans fatty acids programmed the hypothalamic feeding control mechanisms. As young adults, only trans-control animals showed loss of insulin-induced hypophagia, indicating that the mismatch between early and later nutritional environments was relevant. However, the trans group also showed signs of altered appetite signaling mechanisms, suggesting that the early adaptations may have deleterious consequences later in life.     

Effects of feeding fat during pregnancy and lactation on growth performance, milk composition and very low density lipoprotein composition in ratstc "density lipoprotein composition in rats"

The effects of dietary fat during pregnancy and lactation on growth performance of pups, milk composition and very low density lipoprotein composition in rats were studied. A total of 33 dams were used in this study and each litter was adjusted to 8 pups per dam. The dams were fed on high fat (150 g fat/kg diet, HF), medium fat (75 g fat/kg of diet, MF) and low fat (2.5 g fat/kg diet, LF) diets. The body weights of dams increased during pregnancy and decreased after pregnancy. The HF pups had a higher body weight and higher weight gain than those of LF pups. The amount of feed intake of HF dams was significantly higher than LF and MF dams. The HF dams had significantly higher milk fat and water concentrations than LF dams. The milk protein was not significantly different among the treatment groups. All dams showed hypertriacylglycerolaemia in their very low density lipoprotein (VLDL) in late pregnancy. The VLDL-protein concentrations increased during the first week after parturition. The HF dams showed a greater response to the dietary fat than that of LF and MF dams. The findings suggest that addition of fat in the diet during pregnancy and lactation may improve the milk quality through modifying the composition of VLDL contents, leading to better growth of pups.