Junk Food Diet Research Articles

Sex and age-dependent effects of a maternal junk food diet on the mu-opioid receptor in rat offspring

Perinatal junk food exposure increases the preference for palatable diets in juvenile and adult rat offspring. Previous studies have implicated reduced sensitivity of the opioid pathway in the programming of food preferences; however it is not known when during development these changes in opioid signalling first emerge. This study aimed to determine the impact of a maternal junk food (JF) diet on mu-opioid receptor (MuR) expression and ligand binding in two key regions of the reward pathway, the nucleus accumbens (NAc) and the ventral tegmental area (VTA) in rats during the early suckling (postnatal day (PND) 1 and 7) and late suckling/early post-weaning (PND 21 and 28) periods. Female rats were fed either a JF or a control diet for two weeks prior to mating and throughout pregnancy and lactation. MuR expression in the VTA was significantly reduced in female JF offspring on PND 21 and 28 (by 32% and 57% respectively, P<0.05), but not at earlier time points (PND 1 and 7). MuR ligand binding was also reduced (by 22%, P<0.05) in the VTA of female JF offspring on PND 28. No effects of perinatal junk food exposure on MuR mRNA expression or binding were detected at these time points in male offspring. These findings provide evidence that the opioid signalling system is a target of developmental programming by the end of the third postnatal week in females, but not in males.

Assessing the Primary Causes of Hypertension in Khyber Pakhtunkhwa, Pakistan

Hypertension also called a silent killer is a serious problem. The numbers of hypertensive patients are increasing day by day. The present study aim to assess the primary causes of hypertension in Khyber Pakhtunkhwa. Data for the study were collected from 298 hypertensive patients who were admitted or visited to Hayatabad Medical Complex Peshawar as patients. Simple random sampling method was used for selection of the sampled respondents. The results indicate a significant association between hypertension and the level of education (P=.000). Educated people were found not only having more information about hypertension but also found more conscious about the disease (P=.000), while no or low level of educated patients were reported not only caring (P.000) the hypertension but also were not consulting doctors (P=.000). Sampled hypertensive patients were also agreed that regular use of antihypertensive medicines (P=.000), easy supply of medicines (P=.001), regular exercise (P=.000) and regular check-up of blood pressure (P.000) can help maintain blood pressure in normal range while irregularity in taking of medicines (P=.000) and sedentary life style (P=.000) contributed to high blood pressure. Dietary habits (P=.005) such as junk food (P=.000) and spicy diet (P.000) reported affected the blood pressure. Regarding precautions significant association was found with life style modification (P=.000), regular check-up of blood pressure (P=.000), regular exercise (P=.036), weight reduction (P=.001), avoid alcohol consumption (P=.000), stopped smoking (P=.000) and avoid stress (P=.002) along with more use of vegetables and fruits (P=.001). On the other hand hypertension was also associated significantly with the people who have obesity (P=.004), lake of exercise P=.000), old people (P=.034), low socio-economic status (P=.000), kidney diseases (P=.000), endocrine diseases (P=.000), excessive salt intake (P=.008), low potassium intake (P=.010) and family history (P=.001). Individually and psychologically the hypertension can also be due to alcohol intake (P=.000), cigarette smoking (P=.000), sedentary life style (P=.000), lake of exercise (P=.000), lake of knowledge about the signs, symptoms of hypertension (P=.000), its causes (P=.000), and precautions (P=.000). Study recommends that in order to control hypertension, a special attention is needed to follow the precautions about hypertension, diet plan, regular check-up of blood pressure, awareness about the disease and avoid stress.

Individual Differences in Cue-Induced Motivation and Striatal Systems in Rats Susceptible to Diet-Induced Obesity.

Pavlovian cues associated with junk-foods (caloric, highly sweet, and/or fatty foods), like the smell of brownies, can elicit craving to eat and increase the amount of food consumed. People who are more susceptible to these motivational effects of food cues may have a higher risk for becoming obese. Further, overconsumption of junk-foods leading to the development of obesity may itself heighten attraction to food cues. Here, we used a model of individual susceptibility to junk-foods diet-induced obesity to determine whether there are pre-existing and/or diet-induced increases in attraction to and motivation for sucrose-paired cues (ie, incentive salience or 'wanting'). We also assessed diet- vs obesity-associated alterations in mesolimbic function and receptor expression. We found that rats susceptible to diet-induced obesity displayed heightened conditioned approach prior to the development of obesity. In addition, after junk-food diet exposure, those rats that developed obesity also showed increased willingness to gain access to a sucrose cue. Heightened 'wanting' was not due to individual differences in the hedonic impact ('liking') of sucrose. Neurobiologically, Mu opioid receptor mRNA expression was lower in striatal 'hot-spots' that generate eating or hedonic impact only in those rats that became obese. In contrast, prolonged exposure to junk-food resulted in cross-sensitization to amphetamine-induced locomotion and downregulation of striatal D2R mRNA regardless of the development of obesity. Together these data shed light on individual differences in behavioral and neurobiological consequences of exposure to junk-food diets and the potential contribution of incentive sensitization in susceptible individuals to greater food cue-triggered motivation.

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.

Early Life Factors and Type 2 Diabetes Mellitus

Type 2 diabetes mellitus (T2DM) is a multifactorial disease, and its aetiology involves a complex interplay between genetic, epigenetic, and environmental factors. In recent years, evidences from both human and animal experiments have correlated early life factors with programming diabetes risk in adult life. Fetal and neonatal period is crucial for organ development. Many maternal factors during pregnancy may increase the risk of diabetes of offsprings in later life, which include malnutrition, healthy (hyperglycemia and obesity), behavior (smoking, drinking, and junk food diet), hormone administration, and even stress. In neonates, catch-up growth, lactation, glucocorticoids administration, and stress have all been found to increase the risk of insulin resistance or T2DM. Unfavorable environments (socioeconomic situation and famine) or obesity also has long-term negative effects on children by causing increased susceptibility to T2DM in adults. We also address the potential mechanisms that may underlie the developmental programming of T2DM. Therefore, it might be possible to prevent or delay the risk for T2DM by improving pre- and/or postnatal factors.

A maternal “junk‐food” diet reduces sensitivity to the opioid antagonist naloxone in offspring postweaning

Perinatal exposure to a maternal "junk-food" diet has been demonstrated to increase the preference for palatable diets in adult offspring. We aimed to determine whether this increased preference could be attributed to changes in μ-opioid receptor expression within the mesolimbic reward pathway. We report here that mRNA expression of the μ-opioid receptor in the ventral tegmental area (VTA) at weaning was 1.4-fold (males) and 1.9-fold (females) lower in offspring of junk-food (JF)-fed rat dams than in offspring of dams fed a standard rodent diet (control) (P<0.05). Administration of the opioid antagonist naloxone to offspring given a palatable diet postweaning significantly reduced fat intake in control offspring (males: 7.7 ± 0.7 vs. 5.4 ± 0.6 g/kg/d; females: 6.9 ± 0.3 vs. 3.9 ± 0.5 g/kg/d; P<0.05), but not in male JF offspring (8.6 ± 0.6 vs. 7.1 ± 0.5 g/kg/d) and was less effective at reducing fat intake in JF females (42.2 ± 6.0 vs. 23.1 ± 4.1% reduction, P<0.05). Similar findings were observed for total energy intake. Naloxone treatment did not affect intake of standard rodent feed in control or JF offspring. These findings suggest that exposure to a maternal junk-food diet results in early desensitization of the opioid system which may explain the increased preference for junk food in these offspring.

Transversal analysis of junk food diet for a group of medical students and its association with metabolic syndrome

Abstract Objective: to evaluate the nutritional behavior of medical students regarding junkfood intake in relation with the metabolic syndrome (MS). Material and Method:

Are Soda-Swilling Teens More Apt to Be Violent?

Are Soda-Swilling Teens More Apt to Be Violent?

Effect of high-fat diet on stress responsiveness in borderline hypertensive rats

Stress in combination with genetic susceptibility is a factor in the development of hypertension. We used borderline hypertensive rats to investigate whether exposure to high-fat and/or junk-food diet at different stages of ontogeny has programing consequences on stress responses. Wistar dams were fed a high- or low-fat diet for 6 weeks prior to mating with spontaneously hypertensive males, and during gestation. At birth, litters were fostered either to a dam in the same or an alternative diet condition as during gestation. After weaning, male offspring were fed either a control-chow diet or an intermittent junk food fatty diet. Between postnatal days 57–61, half of the rats in each dietary group received daily social defeat sessions using a resident-intruder protocol, and the other half were unstressed controls. Blood pressure was measured indirectly both before and after each defeat session. On the final day, rats were killed for physiological measures. Socially defeated rats showed large increases in serum corticosterone concentration and adrenal hypertrophy, indicating the effectiveness of this non-adapting stressor. Serum corticosterone level was also higher in rats fed with the junk-food diet post-weaning compared with those fed with chow only, but there were no significant effects of gestational or lactational dietary history.

A Maternal “Junk Food” Diet in Pregnancy and Lactation Promotes Nonalcoholic Fatty Liver Disease in Rat Offspring

With rising obesity rates, nonalcoholic fatty liver disease is predicted to become the main cause of chronic liver disease in the next decades. Rising obesity prevalence is attributed to changes in dietary habits with increased consumption of palatable junk foods, but maternal malnutrition also contributes to obesity in progeny. This study examines whether a maternal junk food diet predisposes offspring to nonalcoholic fatty liver disease. The 144 rat offspring were fed either a balanced chow diet alone or with palatable junk foods rich in energy, fat, sugar, and/or salt during gestation, lactation, and/or after weaning up to the end of adolescence. Offspring fed junk food throughout the study exhibited exacerbated hepatic steatosis, hepatocyte ballooning, and oxidative stress response compared with offspring given free access to junk food after weaning only. These offspring also displayed sex differences in their hepatic molecular metabolic adaptation to diet-induced obesity with increased expression of genes associated with insulin sensitivity, de novo lipogenesis, lipid oxidation, and antiinflammatory properties in males, whereas the gene expression profile in females was indicative of hepatic insulin resistance. Hepatic inflammation and fibrosis were not detected indicating that offspring had not developed severe steatohepatitis by the end of adolescence. Hepatic steatosis and increased oxidative stress response also occurred in offspring born to junk food-fed mothers switched to a balanced chow diet from weaning, highlighting a degree of irreversibility. This study shows that a maternal junk food diet in pregnancy and lactation contributes to the development of nonalcoholic fatty liver disease in offspring.

Does Junk Food Lead to Heart Failure?

Experimental and clinic studies show that chronic hypertension leads to myocardial pathology and systolic and diastolic dysfunctions that frequently progress to heart failure.1 Elevated afterload causes cardiomyocyte hypertrophy, which alters myocardial energy metabolism by increasing glucose metabolism and impairing mitochondrial oxidative capacity, increasing the production of reactive oxygen species and oxidative damage, and triggering remodeling of the myocardial extracellular matrix and the left ventricle (see Figure).2 Obesity is also a strong risk factor for both hypertension and heart failure and has been increasing at epidemic proportions worldwide.3,4 The increase in obesity in Western societies over the last century is associated with greater consumption of highly processed carbohydrates (eg, sugar, white flour, and white potatoes) and saturated fats.5 At present, there is little information regarding the effects of dietary fat and carbohydrate composition on cardiac function and the development of heart failure in hypertension. Figure. Schematic depiction of the potential impact of a junk-food diet on the development of cardiac pathology essential hypertension. A diet high in sugar, high-glycemic starch, and saturated fats promotes myocardial dysfunction through hypertension and obesity-dependent and -independent pathways. ROS indicates reactive oxygen species. In the present issue of Hypertension , Majane et al6 present the novel finding that consuming a diet that is high in sugar and saturated fat results in relative modest obesity (≈10% increase in body mass) compared with a sugar-free, low-fat diet but greatly accelerates left ventricular dysfunction in a …

Maternal nutritional history predicts obesity in adult offspring independent of postnatal diet

Maternal nutritional history predicts obesity in adult offspring independent of postnatal diet

Evidence that a maternal “junk food” diet during pregnancy and lactation can reduce muscle force in offspring

Obesity is a multi-factorial condition generally attributed to an unbalanced diet and lack of exercise. Recent evidence suggests that maternal malnutrition during pregnancy and lactation can also contribute to the development of obesity in offspring. We have developed an animal model in rats to examine the effects of maternal overeating on a westernized "junk food" diet using palatable processed foods rich in fat, sugar and salt designed for human consumption. Using this model, we have shown that such a maternal diet can promote overeating and a greater preference for junk food in offspring at the end of adolescence. The maternal junk food diet also promoted adiposity and muscle atrophy at weaning. Impaired muscle development may permanently affect the function of this tissue including its ability to generate force. The aim of this study is to determine whether a maternal junk food diet can impair muscle force generation in offspring. Twitch and tetanic tensions were measured in offspring fed either chow alone (C) or with a junk food diet (J) during gestation, lactation and/or post-weaning up to the end of adolescence such that three groups of offspring were used, namely the CCC, JJC and JJJ groups. We show that adult offspring from mothers fed the junk food diet in pregnancy and lactation display reduced muscle force (both specific twitch and tetanic tensions) regardless of the post-weaning diet compared with offspring from mothers fed a balanced diet. Maternal malnutrition can influence muscle force production in offspring which may affect an individual's ability to exercise and thereby combat obesity.

Effect of high-fat diet during gestation, lactation, or postweaning on physiological and behavioral indexes in borderline hypertensive rats

Maternal obesity is becoming more prevalent. We used borderline hypertensive rats (BHR) to investigate whether a high-fat diet at different stages of development has adverse programming consequences on metabolic parameters and blood pressure. Wistar dams were fed a high- or low-fat diet for 6 wk before mating with spontaneously hypertensive males and during the ensuing pregnancy. At birth, litters were fostered to a dam from the same diet group as during gestation or to the alternate diet condition. Female offspring were weaned on either control or "junk food" diets until about 6 mo of age. Rats fed the high-fat junk food diet were hyperphagic relative to their chow-fed controls. The junk food-fed rats were significantly heavier and had greater fat pad mass than those rats maintained on chow alone. Importantly, those rats suckled by high-fat dams had heavier fat pads than those suckled by control diet dams. Fasting serum leptin and insulin levels differed as a function of the gestational, lactational, and postweaning diet histories. Rats gestated in, or suckled by high-fat dams, or maintained on the junk food diet were hyperleptinemic compared with their respective controls. Indirect blood pressure did not differ as a function of postweaning diet, but rats gestated in the high-fat dams had lower mean arterial blood pressures than those gestated in the control diet dams. The postweaning dietary history affected food-motivated behavior; junk food-fed rats earned less food pellets on fixed (FR) and progressive (PR) ratio cost schedules than chow-fed controls. In conclusion, the effects of maternal high-fat diet during gestation or lactation were mostly small and transient. The postweaning effects of junk food diet were evident on the majority of the parameters measured, including body weight, fat pad mass, serum leptin and insulin levels, and operant performance.

Highlights From The Literature

Highlights From The Literature

Offspring from mothers fed a 'junk food' diet in pregnancy and lactation exhibit exacerbated adiposity that is more pronounced in females.

We have shown previously that a maternal junk food diet during pregnancy and lactation plays a role in predisposing offspring to obesity. Here we show that rat offspring born to mothers fed the same junk food diet rich in fat, sugar and salt develop exacerbated adiposity accompanied by raised circulating glucose, insulin, triglyceride and/or cholesterol by the end of adolescence (10 weeks postpartum) compared with offspring also given free access to junk food from weaning but whose mothers were exclusively fed a balanced chow diet in pregnancy and lactation. Results also showed that offspring from mothers fed the junk food diet in pregnancy and lactation, and which were then switched to a balanced chow diet from weaning, exhibited increased perirenal fat pad mass relative to body weight and adipocyte hypertrophy compared with offspring which were never exposed to the junk food diet. This study shows that the increased adiposity was more enhanced in female than male offspring and gene expression analyses showed raised insulin-like growth factor-1 (IGF-1), insulin receptor substrate (IRS)-1, vascular endothelial growth factor (VEGF)-A, peroxisome proliferator-activated receptor-gamma (PPARgamma), leptin, adiponectin, adipsin, lipoprotein lipase (LPL), Glut 1, Glut 3, but not Glut 4 mRNA expression in females fed the junk food diet throughout the study compared with females never given access to junk food. Changes in gene expression were not as marked in male offspring with only IRS-1, VEGF-A, Glut 4 and LPL being up-regulated in those fed the junk food diet throughout the study compared with males never given access to junk food. This study therefore shows that a maternal junk food diet promotes adiposity in offspring and the earlier onset of hyperglycemia, hyperinsulinemia and/or hyperlipidemia. Male and female offspring also display a different metabolic, cellular and molecular response to junk-food-diet-induced adiposity.

P2-128 The influence of a maternal junk food diet on the feeding behaviour and growth of the offspring

P2-128 The influence of a maternal junk food diet on the feeding behaviour and growth of the offspring

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.

Brown (BAT) and white (WAT) adipose tissue in high-fat junk food (HFJF) and chow-fed rats with dorsomedial hypothalamic lesions (DMNL rats)

Male weanling rats received dorsomedial hypothalamic nucleus lesions (DMNL) or sham operations and were fed for 173 postoperative days a high-fat diet and given a 32% sucrose solution as drinking fluid. This was supplemented with chocolate chip cookies, potato chips and marshmallows. Other DMNL and sham-operated controls were fed lab chow instead of the above high-fat junk food diet (HFJF) and given tap water instead of 32% sucrose solution. All animals were killed on postoperative day 174. Caloric intake per 100 g body weight was similar in all groups; however, the HFJF fed control and DMNL rats had significantly elevated carcass fat. Since HFJF-DMNL rats were not nearly as obese as the HFJF control animals, it appears that the DMNL offered some protection against the HFJF-diet-produced obesity. When their smaller body size is considered. DMN lesions had no effect on brown adipose tissue (BAT) mass in chow-fed or HFJF fed rats, whereas BAT size was significantly enlarged in HFJF-fed control animals. This suggests but does not prove that HFJF-fed controls, but not DMNL rats, may be using dietary-induced thermogenesis (DIT) to attenuate their obesity. We hypothesize that the HFJF-fed DMNL may not be enhancing DIT as reflected in normal BAT size, because they had not attained a degree of fatness to activate this system, or the DMN lesions impaired its activation. Both HFJF-fed groups showed reduced linear growth compared to their counterparts. The reason for stunting is uncertain, but may be related to their low plasma insulin concentrations.

Heart and liver lipid fatty acid and behavior changes in mice after a diet change

270-Day old, male Ham/ICR mice were subjected to a diet change from high protein and carbohydrate and low fat to a diet higher in fat and lower in carbohydrate and protein. Age matched mice were maintained on laboratory rodent chow as controls. The diet change was not defined so the observed differences could not necessarily be ascribed to altered protein, carbohydrate, or fat intake. Comparison of the controls with the experimental mice revealed the “junk food” mice differed in lipid fatty acid profiles of the heart and liver and in percentage of lipid palmitic and oleic acids in these organs and also in plasma. Appearance was altered in the experimental mice which had dull, greasy coats. In addition, the experimental animals were less active, slept singly, and were slower in negotiating a three-choice maze than their comparably housed counterparts, indicating altered activity/curiosity behavior. It has been clearly demonstrated that dietary manipulation affects many aspects of body function in animals and humans. For example, nutrition and/or caloric intake affects kidney disease (1), myocardial fibrosis (2), the prevalence of neoplasms (3), learning behavior in rats (4,5), immunological function in mice (6), liver metabolism as exemplified by diet regulated lipogenic activity in rat liver (7–10), morphological effects on the central nervous system (11), and hepatic enzyme activity (12). An intriguing effect of diet is it possible role in aging. Increased longevity in rodents is clearly correlated with certain early diet deprivations (13,2). Rapid growth rate appears to have an adverse effect on longevity, and some typical biochemical changes associated with aging are delayed by a restricted diet. There may also be mesureable biochemical links between diet and quality of life in terms of function. Harmon (14) fed rats from 2 months to senescence (up to 35 months) diets varied in saturated fats. There was no effect on longevity, but the higher the unsaturated fat content in the diet, the worse the performance of the animal in a closed field maze. It was speculated that increased unsaturation in lipid membranes increased suseptibility to free radical damage which affected CNS function. It is not clear why the presumed stimulation of lipid peroxidation by the presence of unsaturated fats did not have an effect on longevity, as one might reasonably assume that the adverse effects on membranes caused by lipid ixidation would promote neoplasms, organs dysfunction, and disease. Body lipids appear to play a role in quality of life and, possibly, aging, particularly in their important role in membrane function. Therefore, it seemed useful to document the response of heart, liver, and plasma lipids to a sudden diet change in a fully mature animal where maturation processes were not a factor. In addition, a “supermarket” diet (15) was used with the idea it would parallel the eating habits of some middle age Americans. The unexpected results of this preliminary study were a marked change in curiosity/activity behavior and a dramatic change in appearance of the mice on the junk food diet. Also found were highly significant increases in specific lipids in the heart and liver as well as in the percent of oleic and palmitic acids in plasma and in some classes of heart and liver lipids.