Fat Calories Research Articles

Supra-Additive Effects of Combining Fat and Carbohydrate on Food Reward

Post-ingestive signals conveying information about the nutritive properties of food are critical for regulating ingestive behavior. Here, using an auction task concomitant to fMRI scanning, we demonstrate that participants are willing to pay more for fat+ carbohydrate compared with equally familiar, liked, and caloric fat or carbohydrate foods and that this potentiated reward is associated with response in areas critical for reward valuation, including the dorsal striatum and mediodorsal thalamus. We also show that individuals are better able to estimate the energy density of fat compared with carbohydrate and fat+ carbohydrate foods, an effect associated with functional connectivity between visual (fusiform gyrus) and valuation (ventromedial prefrontal cortex) areas. These results provide the first demonstration that foods high in fat and carbohydrate are, calorie for calorie, valued more than foods containing only fat or carbohydrate and that this effect is associated with greater recruitment of central reward circuits.

Effects of Green Tea (Sliming Herbal Tea) and Role of Dietary Practice to Reduce Obesity

Obesity is a cluster of non-transmissible diseases creating a massive socioeconomic and civil health burden in both developed and developing countries. The prevalence of obesity is increased in an alarming rate and one-third of the world’s population carrying obesity. Phenolic compounds from plant sources play a great role on obesity. Green tea or herbal tea that contains four types of catechins reduced cholesterol level through the modulation of bile acid absorption and metabolism.
 Objectives: the aim of this study was to monitor the effects of green tea and nutritional education about dietary habit on obese persons.
 Methods: A randomized control trial (n=20) of obese persons were selected as baseline study and a sliming herbal tea (green tea) with nutritional counseling was prescribed for 12 weeks to take regularly for twice in a day. Results: This study showed a positive impact on obese individuals. After 12 weeks intervention, BMI was decreased from 30.94 to 30.57, body weight, body fat and body fat mass were reduced from 72.50 to 71.36 kg, 32.06 to 30.18% and 27.38 to 25.52 kg respectively. Moreover, a dietary practice of high protein diet with low calorie and low fat diet was developed through nutrition counseling at the baseline study. Conclusion: Obesity management is a combined process. So, green tea with planned diet might be a fruitful effort to reduce body weight, body fat and overall BMI of an obese person.

Nutrient‐specific compensation for seasonal cold stress in a free‐ranging temperate colobine monkey

Abstract Homeostatic responses of animals to environmentally induced changes in nutrient requirements provide a powerful basis for predictive ecological models, and yet, such responses are virtually unstudied in the wild. We tested for macronutrient‐specific compensatory feeding responses by free‐ranging golden snub‐nosed monkeys (Rhinopithecus roxellana) inhabiting high altitude temperate forests, where they experience a substantial difference in ambient temperature in cold winters vs. warmer springs. The monkeys had free access to natural foods throughout the year, and to ensure that any seasonal differences in nutrient intake were due to homeostatic compensation and not constraints on food availability, we studied the monkeys during periods in which they were provisioned with the same amount of supplementary foods in winter and spring. Thermoregulatory energy costs in winter and spring were calculated using partitional calorimetric estimations of convective and radiative heat loss obtained from thermal imaging of free‐ranging monkeys in situ. Daily nutrient intakes were measured using continuous focal follows (average 6.9 hr/day) of free‐ranging individuals (27 days in spring and 28 days in winter). We used a nutritional geometry framework to integrate these data and test three predictions: (a) In order to remain thermoneutral (balance heat loss with heat expenditure), golden snub‐nosed monkeys increase daily energy consumption during the winter compared to spring; (b) this increase is achieved specifically by increasing intake of the primary energetic nutrients, carbohydrate and lipid, relative to protein; and (c) the seasonal increase in ingested fat and carbohydrate calories will quantitatively match the additional thermoregulatory costs in winter compared with spring. Our results showed that daily metabolisable energy intake in winter (721.5 kJ/mbm) was 1.8 times that in spring (399 kJ/mbm). As predicted, this difference was specific to fat and carbohydrate, whereas seasonal protein intake did not differ significantly. Winter consumption of fat and carbohydrate was 326 kJ/mbm per day greater than in spring, a value that closely matched the seasonal difference in the daily energetic costs of thermoregulation (329 kJ/mbm). This is the first study to test for a match between nutrient‐specific homeostatic compensation and environmentally induced perturbations in nutrient requirements in free‐ranging animals and underpins the potential for the homeostasis framework to provide predictive power to ecological models.

Metabolic and Weight Changes After Bariatric Surgery in a Rat Model of Induced Type 2 Diabetes Mellitus and Obesity

Sleeve gastrectomy (SG) and gastric plication (GP) are surgical procedures providing weight loss through several mechanisms incompletely understood. Rat models allow the possibility of tight regulation of experimental conditions, making them the ideal candidates for animal models in bariatric surgery. The aim of this study was to compare the weight and metabolic changes between sleeve gastrectomy and gastric plication in a rat model with type 2 induced diabetes mellitus and obesity. Fifteen male Wistar rats were fed with DIO food (Bio Serv �F3282 - Mouse Diet, High Fat, Fat Calories -60%), after 36 weeks were allocated to the study three arms-SG, GP and sham operation (SO). Four weeks after the surgery the rats were weighted again. Blood tests were performed before surgery and four weeks after surgery searching for blood glucose, total cholesterol, HDL, triglycerides, and LDL. At the onset of the study, the rats were 9 weeks old and had an average body mass of 231.6g � 31.58. After 36 weeks of DIO, one day preoperatively body weight was 774.93g � 95.02. The preoperatively average of body weight in the SG group was 777.4g �104.66, 775.4 g �104.6 in the GP group, respectively 772g �79 in the SO group. 4 weeks after surgery the mean body weight in the SG group was 648.8g �99.09, in the GP group was 695.6g �99.09, respectively 825.4g �79.87 in the SO fed ad libitum group. There was a significant decrease of mean fasting glucose levels at 4 weeks postoperative in the SG group compared to the SO group (87.4mg/dL�8.73 versus 103.6 mg/dlL�4.66, p= 0.01). The same trend of mean fasting glucose was registered in the GP group versus the SO group (92.8 � 5.67 mg/dl vs 103.6 mg/dl � 4.66, p=0.01). Our study provides evidence of the positive effects of bariatric surgery for treating patients with morbid obesity associated with diabetes mellitus and dyslipidemia and the use of rats to study the mechanisms of weight reduction and metabolic changes in bariatric surgery.

Lack of a‐CGRP Prevents High Fat Diet Induced Biliary Proliferation and Hepatic Steatosis

Nonalcoholic fatty liver disease (NAFLD) has become a prevalent problem in westernized societies where incidents of obesity lead to a reduction in blood flow and a deposition of fat into the liver increasing incidents of maladies ranging from minor nonclinical hepatic steatosis (NASH) to severe cirrhosis and cholangiocarcinoma (CCA). We have previously shown that cholangiocytes participate in a sub epithelial fibrotic process that is the hallmark of hepatobiliary injury. Employing a well‐established mouse model of mechanical liver injury through bile duct ligation (BDL), we have shown that cholangiocytes are regulated, in part, through sensory innervation, and manipulation of the innervation pathway through a‐calcitonin gene‐related peptide (a‐CGRP) signaling results in a reduction in cholangiocyte proliferation as well as liver fibrosis. Due to the fibrotic nature of fatty liver disease and our previous research demonstrating the interplay between cholangiocytes, neuropeptides, and sensory receptors, we AIM to evaluate the role a‐CGRP plays in the biliary progression from hepatic steatosis to the profibrotic phenotype found in the damaged biliary epithelium.METHODSStudies were performed in C57 (WT) and CGRP KO mice (4 wk of age). Mice were treated with Control and High Fat Diet (0.2% cholesterol, 45% fat calories, with 30% of the fat in the form of partially hydrogenated vegetable oil) with 45% fructose, 55% glucose (42g/L) drinking water for 20 wks. Fat deposition was visualized via Oil Red O staining. Ductular reaction (IBDM), CGRP accessory protein and collagen deposition was evaluated by IHC for CK‐19, RAMP1 and Sirius Red, respectively, in total liver sections. a‐CGRP was evaluated via protein expression in mouse total liver and mRNA in human tissue by IHC and qPCR. mRNA data for CLR, CALCRL, RAMP1, and CGRP was obtained via qPCR in pure cholangiocytes in WT CD and WT HFD.RESULTSThere was a significant decrease in the fat deposition in the a‐CGRP KO HFD compared to the WT HFD. There was a significant decrease in IBDM and collagen deposition in CGRP KO HFD mice compared to WT HFD. Both mouse HFD and human steatotic livers showed significant increases in a‐CGRP when compared to their WT counterpart. Additionally, IHC demonstrated a significant increase in RAMP1 in the WT HFD when compared to CD. Cholangiocytes had significant increase in the expression of mRNA in the CGRP receptor (CLR), the receptor component (CGRPRC), its accessory, RAMP1, and the protein CGRP in HFD when compared to the WT CD.CONCLUSIONa‐CGRP plays a substantial role in proliferation and hepatic fibrosis. Modulation of the a‐CGRP axis may represent a novel therapeutic approach for the management of NAFLD.Support or Funding InformationNIH R01 DK76898This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Comparison of Children's Menu Items at Full- and Quick-Service Restaurants.

The proportion of food consumed by children from restaurants tripled during the last 4 decades and that coincided with the increased rate of obesity. Despite the presence of data linking quick-service (QS) food consumption to poor diet quality, studies comparing the nutrition content of the children's menu items at QS restaurants (QSRs) with those at full-service restaurants (FSRs) are limited. The objectives of this study were to examine the nutrition content of common children's menu items at both QSRs and FSRs and compare these data with recommendations reported by the Dietary Guidelines for Americans 2015-2020, Eighth Edition. Using the 2014 data of the MenuStat project, 10 food items that are on both QSR and FSR children's menus were selected. Data from each restaurant category were aggregated and the overall average of the nutritional content of each individual food item was calculated and compared between the two restaurant categories. The average of calories, fat, carbohydrates, and added sugar of most items on the children's menu of QSRs are lower than those of FSRs. Also, most food items on children's menus of FSRs, and to a lesser extent those of QSRs, exceeded the national recommended calories and fat content per meal. Although some children's menu items of QSRs have less fat and fewer calories compared with those of FSRs, most menu items in both FSRs and QSRs do not meet national dietary recommendations. Healthcare professionals may expand discussions with patients to include both restaurant categories when counseling them and their families on obesity prevention. Also, educating children and families about reading the nutritional content information of children's menu items when eating out to make an informed choice can be a tool in fighting childhood obesity.

Formulation of Emergency Food in Biscuit-Form Made From Proso Millet Flour (Panicum miliaceum) and Snakehead Fish (Channa striata) –Tempeh Flour Koya

Indonesia is a natural disaster-prone country. Food availability appears as the post-disaster main problem. Emergency food is an effort to overcome it. An ideal emergency food is expected to have a complete nutritional composition. Fulfilling macronutrient needs, proso millet flour and snakehead fish-tempeh flour koya were being used in this research. The objective of this research was to determine the formulation of emergency food in biscuit form made from proso millet flour and snakehead fish-tempeh flour koya based on its sensory, chemical and physical properties. This research was using a completely randomized design with one factor affecting. The variations of proso millet flour and snakehead fish-tempeh flour koya composition were 100:0 ; 80:20 ; 60:40 ; and 40:60. All treatments were carried out sensory evaluation using hedonic test, proximate analysis, calories analysis using bomb calorimetry methods. and physical analysis using texture profile analyzer. The compensatory model was used to determine the best formula based on all parameters. The result indicated that the best biscuit formula had compositions of proso millet flour 80% and snakehead fish-tempeh flour koya 20%. It had a brownish color, not-strong-fishy aroma, a strong-enough bitter aftertaste and crunchy texture. Chemical analysis showed that its moisture, ash, protein, fat, carbohydrate and total calories content were 1,146%; 4,827%; 12,536%; 26,325%; 56,312% and 5,033 kcal/gram, respectively. The physical analysis shows that its hardness and fracturability values were 8,037 N and 2,403 N, respectively.

Catecholaminergic projections into an interconnected forebrain network control the sensitivity of male rats to diet-induced obesity

Hindbrain catecholamine neurons convey gut-derived metabolic signals to an interconnected neuronal network in the hypothalamus and adjacent forebrain. These neurons are critical for short-term glycemic control, glucocorticoid and glucoprivic feeding responses, and glucagon-like peptide 1 (GLP-1) signaling. Here we investigate whether these pathways also contribute to long-term energy homeostasis by controlling obesogenic sensitivity to a high-fat/high-sucrose choice (HFSC) diet. We ablated hindbrain-originating catecholaminergic projections by injecting anti-dopamine-β-hydroxylase-conjugated saporin (DSAP) into the paraventricular nucleus of the hypothalamus (PVH) of male rats fed a chow diet for up to 12 wk or a HFSC diet for 8 wk. We measured the effects of DSAP lesions on food choices; visceral adiposity; plasma glucose, insulin, and leptin; and indicators of long-term ACTH and corticosterone secretion. We also determined lesion effects on the number of carbohydrate or fat calories required to increase visceral fat. Finally, we examined corticotropin-releasing hormone levels in the PVH and arcuate nucleus expression of neuropeptide Y ( Npy), agouti-related peptide ( Agrp), and proopiomelanocortin ( Pomc). DSAP-injected chow-fed rats slowly increase visceral adiposity but quickly develop mild insulin resistance and elevated blood glucose. DSAP-injected HFSC-fed rats, however, dramatically increase food intake, body weight, and visceral adiposity beyond the level in control HFSC-fed rats. These changes are concomitant with 1) a reduction in the number of carbohydrate calories required to generate visceral fat, 2) abnormal Npy, Agrp, and Pomc expression, and 3) aberrant control of insulin secretion and glucocorticoid negative feedback. Long-term metabolic adaptations to high-carbohydrate diets, therefore, require intact forebrain catecholamine projections. Without them, animals cannot alter forebrain mechanisms to restrain increased visceral adiposity.

A predictive model of rat calorie intake as a function of diet energy density.

Easy access to high-energy food has been linked to high rates of obesity in the world. Understanding the way that access to palatable (high fat or high calorie) food can lead to overconsumption is essential for both preventing and treating obesity. Although the body of studies focused on the effects of high-energy diets is growing, our understanding of how different factors contribute to food choices is not complete. In this study, we present a mathematical model that can predict rat calorie intake to a high-energy diet based on their ingestive behavior to a standard chow diet. Specifically, we propose an equation that describes the relation between the body weight ( W), energy density ( E), time elapsed from the start of diet ( T), and daily calorie intake ( C). We tested our model on two independent data sets. Our results show that the suggested model can predict the calorie intake patterns with high accuracy. Additionally, the only free parameter of our proposed equation (ρ), which is unique to each animal, has a strong correlation with their calorie intake.

Investigation of the relationship between oxidative stress and SCUBE1 levels in high fat diet-induced obese rats

Background/aim: This study aimed to investigate signal peptide-Cub-EGF domain-containing protein 1 (SCUBE1) levels and oxidative stress (OS) in a high fat diet (HFD)-induced obese rat model. Materials and methods: Fourteen rats were randomly divided into two groups. Group 1, the control group, was given a standard diet (10% calories of fat) and Group 2, the obese group, was given a HFD (60% calories of fat), both for 70 days. Rats were then sacrificed and serum samples were collected. Serum glucose and triglyceride concentrations were determined using an autoanalyzer. Serum SCUBE1, adiponectin, and plasminogen activator inhibitor-1 levels were determined using an enzyme-linked immunosorbent assay. Serum malondialdehyde levels and superoxide dismutase and glutathione peroxidase enzyme activities were determined using colorimetric methods. Results: Final body weight was higher in the obese group (P = 0.007). Serum malondialdehyde concentrations were also higher in the obese group (P = 0.021). Serum glutathione peroxidase activities were higher in the control group (P = 0.028). Serum SCUBE1 levels were also higher in the control group (P = 0.038). Conclusion: There may be no connection between the measured OS parameters and SCUBE1. Differences in SCUBE1 levels may therefore be evaluated independently from OS in obesity.

Nutritionally enriched 1,3-diacylglycerol-rich oil: Low calorie fat with hypolipidemic effects in rats

An enzymatic process was developed for the preparation of a nutritionally enriched 1,3-diacylglycerol(DAG)-rich oil from a blend of refined sunflower and rice bran oils. The process involves hydrolysis of vegetable oil blend using Candida cylindracea followed by esterification with glycerol using Lipozyme RM1M. The resultant DAG-rich oil contains 84% of DAG (66% of 1,3-DAG, 18% of 1,2-DAG) and 16% of triacylglycerol (TAG) along with micro nutrients like γ-oryzanol, tocotrienols, tocopherols and phytosterols. Nutritional studies of the DAG-rich oil were conducted in Wistar rats and compared with sunflower oil (SFO). The calorific value of the DAG-rich oil was estimated to be 6.45 Kcals/g as against 9.25 Kcals/g for SFO. The serum and liver cholesterol and TAG levels in rats fed with 1,3-DAG-rich oil were found to be significantly reduced as compared to rats fed diet containing SFO. We conclude that 1,3-DAG-rich oil is a low calorie fat and exhibits hypolipidemic effects.

Looking Past the Indian Calorie Debate: What is Happening to Nutrition Transition in India

We utilise large national household datasets for 1993–1994, 2004–2005 and 2011–2012 to analyse factors influencing changing patterns in per capita calorie consumption in India. Our study findings demonstrate the significance of the disease environment in which people live, with those living in healthy areas having lower calorie consumption than those living in less healthy ones. Calorie intake has been falling in India, but the study findings reveal that fat calorie intake has been rising successively over time among the rural and poorer urban sub-populations raising concerns for policy-makers that non-communicable diseases are expected to rise for these vulnerable population groups.

Abstract 1248: Adult calorie restriction reduces weight gain and mammary tumor incidence in obesity prone MMTV-TFG α mice -

Abstract Obesity is associated with increased risk of postmenopausal breast cancer resulting in recommendations for weight gain prevention and/or weight loss. However, there is little experimental data indicating if calorie restriction (CR) initiated in adulthood impacts mammary tumorigenesis. We have used female MMTV-TGF-α mice which develop mammary tumors in the 2nd yr of life as a model of postmenopausal breast cancer. From 10-30 weeks of age (woa) mice were fed a diet with 33% fat calories. At 30 woa based on body weight mice were classified as Obesity-Prone (Ob-Pr), Overweight (Ow) or Obesity-Resistant (Ob-R). Half in each weight category were then fed a 25% CR diet with reduced carbohydrate content (43% fat calories). The remaining mice continued on ad libitum (AL) feeding of the 33% fat diet. This resulted in six experimental groups (n = 26-31/group). Food intakes were monitored and body weights and mammary tumor status were determined weekly. Mice were sacrificed either at 90 woa or earlier if tumor size dictated. Mice in the CR-Ob-Pr group lost an average of 1.12 grams while mice in the AL-Ob-Pr group gained 16.03 grams from 30 woa until euthanasia. CR-Ob-Pr mice had a reduced palpable tumor incidence as compared to AL-Ob-Pr mice prior to euthanasia (12.90% versus 61.54% P = 0.0002). Indolent tumors were discovered at euthanasia with the CR-Ob-Pr mice having a larger number than AL-Ob-Pr mice resulting in final tumor positive mice in these groups of 54.84% vs 65.38%, respectively. Interestingly, the Ob-R mice had final tumor incidence of 38.71% and 73.08% for the CR-Ob-R vs the AL-Ob-R (P<0.01). Average tumor weight was highest in the AL-Ob-Pr group with CR resulting in a significantly lower tumor weight (P< 0.01). The AL-Ob-Pr group had the shortest average survival time of 82.96 woa while CR of the Ob-Pr mice resulted in increased survival to 89.77 woa (P < 0.001). A comparison of the survival curves of these two groups showed that CR resulted in significantly increased survival (P < 0.0001). Results of this study indicate that initiation of moderate 25% CR during adulthood reduces weight gain, mammary tumor incidence, and tumor weight as well as increases lifespan even when a moderately high fat diet was consumed. This information supports further efforts to be made to prevent weight gain as women approach menopause to delay or prevent breast cancer development. Support: NIH-CA157012, The Hormel Foundation and Paint the Town Pink. Citation Format: Michael E. Grossmann, Nancy K. Mizuno, Da-Qing Yang, D. Joshua Liao, Margot P. Cleary. Adult calorie restriction reduces weight gain and mammary tumor incidence in obesity prone MMTV-TFG α mice - [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 1248. doi:10.1158/1538-7445.AM2017-1248

EFFECT OF FOOD ON THE PHARMACOKINETICS OF AZELIRAGON IN HEALTHY ADULT SUBJECTS

Azeliragon, an oral antagonist of the Receptor for Advanced Glycation Endproducts (RAGE), is being evaluated in a pivotal Phase 3 study for efficacy and safety in patients with mild Alzheimer's disease. Azeliragon exerts a multimodal mechanism of action including effects on Aβ, tau phosphorylation, and inflammation through an initial step of blocking proteins (i.e. Aβ, S100b) from binding to RAGE. The present study evaluated the effect of an FDA high fat meal on the pharmacokinetics (PK) of the 5 mg azeliragon Phase 3 capsule formulation. This was an open-label, randomized, parallel, single-dose study to assess the effect of a high-fat meal on the pharmacokinetics of azeliragon. Subjects were randomized to receive a single dose of azeliragon 5 mg administered either following a 10-h overnight fast or within 30 minutes of the start of ingestion of a high fat meal (150 protein calories, 250 carbohydrate calories and 500–600 fat calories). Serial PK samples were collected for 312 hours following dosing. Safety assessments were performed throughout the 14-day study period. Twenty-eight (14 fasted and 14 fed) subjects (27 males, 1 female), 24 to 55 years old, were randomized, and all completed the study. Fed and fasted groups were similar for age, race, ethnicity, height, weight and BMI. Administration with food resulted in an approximately 16–20% reduction in geometric mean estimates of exposure. AUC(0-last) was 113 ng*h/mL fasted and 90 ng/*h/mL fed (ratio: 0.80, 90% CI: 0.57, 1.12). AUC(0–72h) was 38.3 ng*h/mL fasted and 32.0 ng*h/mL fed (ratio: 0.84, 90% CI: 0.70, 1.00). Cmax was 0.70 ng/mL fasted and 0.58 ng/mL fed (ratio: 0.83, 90% CI: 0.69, 1.00). Azeliragon was well tolerated with only 3 mild treatment-emergent adverse events reported (2 in fasted, 1 in fed) none of which resulted in withdrawal from study. There was an approximately 16–20% reduction in exposure (AUC(0-last), AUC(0–72h), Cmax) following administration of azeliragon 5 mg following a high fat meal. At the Phase 3 dose of 5 mg/day the magnitude of reduction is not anticipated to be clinically meaningful. Consequently, azeliragon may be given without regard to meals.

A High-Fructose-High-Coconut Oil Diet Induces Dysregulating Expressions of Hippocampal Leptin and Stearoyl-CoA Desaturase, and Spatial Memory Deficits in Rats.

We investigated the effects of high-fructose-high-fat diets with different fat compositions on metabolic parameters, hippocampal-dependent cognitive function, and brain leptin (as well as stearoyl-CoA desaturase (SCD1) mRNA expressions). Thirty-two male Wistar rats were divided into 3 groups, a control group (n = 8), a high-fructose soybean oil group (37.5% of fat calories, n = 12), and a high-fructose coconut oil group (37.5% of fat calories, n = 12) for 20 weeks. By the end of the study, the coconut oil group exhibited significantly higher serum fasting glucose, fructosamine, insulin, leptin, and triglyceride levels compared to those of the control and soybean oil groups. However, hippocampal leptin expression and leptin receptor mRNA levels were significantly lower, while SCD1 mRNA was significantly higher in rats fed the high-fructose-high-coconut oil diet than in rats fed the other experimental diets. In addition, the coconut oil group spent significantly less time in the target quadrant on the probe test in the Morris water maze (MWM) task. Rats fed the high-fructose-high-coconut oil diet for 20 weeks were prone to develop hyperglycemia, hyperinsulinemia, hyperleptinemia, and hypertriglyceridemia. These metabolic consequences may contribute to hippocampal-dependent memory impairment, accompanied by a lower central leptin level, and a higher SCD1 gene expression in the brain.

Effect of a trans fatty acid-enriched diet on mitochondrial, inflammatory, and oxidative stress parameters in the cortex and hippocampus of Wistar rats.

Previously showed that dietary trans fatty acids (TFAs) may cause systemic inflammation and affect the central nervous system (CNS) in Wistar rats by increased levels of cytokines in the cerebrospinal fluid (CSF) and serum (Longhi et al. Eur J Nutr 56(3):1003-1016, 1). Here, we aimed to clarifying the impact of diets with different TFA concentrations on cerebral tissue, focusing on hippocampus and cortex and behavioral performance. Wistar rats were fed either a normolipidic or a hyperlipidic diet for 90days; diets had the same ingredients except for fat compositions, concentrations, and calories. We used lard in the cis fatty acid (CFA) group and PHSO in the TFA group. The intervention groups were as follows: (1) low lard (LL), (2) high lard (HL), (3) low partially hydrogenated soybean oil (LPHSO), and (4) high partially hydrogenated soybean oil (HPHSO). Mitochondrial parameters, tumor necrosis factor alpha (TNF-α), 2'7'-dichlorofluorescein (DCFH) levels in brain tissue, and open field task were analyzed. A worse brain tissue response was associated with oxidative stress in cortex and hippocampus as well as impaired inflammatory and mitochondrial parameters at both PHSO concentrations and there were alterations in the behavioral performance. In many analyses, there were no significant differences between the LPHSO and HPHSO diets. Partially hydrogenated soybean oil impaired cortical mitochondrial parameters and altered inflammatory and oxidative stress responses, and the hyperlipidic treatment caused locomotor and exploratory effects, but no differences on weight gain in all treatments. These findings suggest that quality is more important than the quantity of fat consumed in terms of CFA and TFA diets.

No association between nutrition and body height in German kindergarten children - a pilot study.

Anthropologists all over the world are discussing influences on individual height including quantity and quality of nutrition. To examine whether a relationship between nutritional components and height can be found this pilot study has been developed. The research samples consisted of 44 children (age 3-6 years) attending two different kindergartens in Germany. Height measurements were taken for each child. Furthermore the parents had to fill out a 24-hour questionnaire to document their children's eating habits during the weekend. In order to standardize the measured height values z-scores were calculated with reference to the average height of the overall cohort. The results of correlation analysis indicate that height is not significantly related to any of the main nutritional components as protein (r = -0.148), carbohydrates (r = 0.126), fat (r = 0.107), fibre (r = -0.289), vitamin (r = 0.050), calcium (r = 0.110), potassium (r = 0.189) and overall calorie intake (r = 0.302). In conclusion, it can be stated that the quality of nutrition may not have a strong influence on individual height. However, due to the small sample size further research should be provided with a larger cohort of children to verify the present results.

Maternal high-fat diet in mice leads to innate airway hyperresponsiveness in the adult offspring.

Maternal obesity prior to and during pregnancy has been associated with an increased incidence of childhood asthma. As diets rich in saturated fat are linked to obesity and inflammation, we created a murine model to investigate the effect of maternal high‐fat diet (HFD) on adult offspring airway hyperreactivity (AHR), a cardinal feature of asthma. Balb/cByJ dams were fed a HFD (60% fat Calories) or normal‐fat diet (NFD) (10% fat Calories) from 8 weeks prior to first breeding through their pregnancies. Pups were weaned to either a HFD or NFD (at 4 weeks of age). AHR was measured in the 10‐week‐old offspring following inhaled methacholine challenge by end‐inflation technique. Bronchial alveolar lavage fluid (BALF) was analyzed for cell count, total protein, and IL‐6. Offspring of HFD dams weaned to NFD had increased AHR compared to offspring of NFD dams weaned to NFD. Offspring of HFD dams that remained on HFDs had increased AHR compared to offspring of NFD dams weaned to HFDs. Offspring of HFD dams had higher BALF cell counts, higher neutrophil percentage, greater total protein, and IL‐6 in the BALF. These results demonstrate that a maternal diet high in saturated fat through pregnancy and lactation plays a key role in programming adult offspring AHR.

Genome-wide analysis identifies colonic genes differentially associated with serum leptin and insulin concentrations in C57BL/6J mice fed a high-fat diet.

Obesity-induced chronic inflammation is known to increase the risk of ulcerative colitis, Crohn’s disease, and colorectal cancer. Accumulating evidence suggests that leptin and insulin are key molecules linking obesity with diseases of the lower intestine. Here, we identified serum phenotype-associated genes in the colon of diet-induced obese mice as early biomarkers of obesity-associated colonic diseases. C57BL/6J mice were fed with either normal diet (ND, 15% of fat calories) or high-fat diet (HFD, 45% of fat calories) for 8 weeks. Serum concentrations of insulin, insulin-like growth factor-1 (IGF-1), leptin, and adiponectin were measured as obesity-related phenotypic markers. Genome-wide gene expression profiles of colon tissue were determined, followed by statistical analyses to detect differentially expressed and serum phenotype-associated genes. HFD-fed mice showed higher serum concentrations of leptin (P < 0.001) and insulin (P < 0.01) than those in the ND group, whereas serum IGF-1 and adiponectin concentrations did not differ between the two dietary groups. Among differentially expressed genes affected by HFD, 135, 128, 110, and 341 genes were associated with serum levels of leptin, insulin, IGF-1, and adiponectin, respectively. We identified 17 leptin-associated genes and 4 insulin-associated genes that inversely responded to HFD and ND. Among these, leptin-associated Peli3 (Pellino E3 ubiquitin protein ligase family member 3), Creb1 (cAMP responsive element binding protein 1), and Enpp2 (ectonucleotide pyrophosphatase/phosphodiesterase 2, autotaxin) and insulin-associated Centg1 (AGAP2, ArfGAP with GTPase domain) are reported to play a role either in obesity or colonic diseases. mRNA expression of these genes was validated by RT-qPCR. Our data suggest Peli3, Creb1, Enpp2, and Centg1 as potential early biomarker candidates for obesity-induced pathophysiological changes in the colon. Future studies verifying the function of these candidates are needed for the prevention, early detection, and treatment of colon diseases.

Infant Adiposity is Independently Associated with a Maternal High Fat Diet but not Related to Niacin Intake: The Healthy Start Study.

Objectives Over-nutrition during pregnancy resulting from maternal obesity or an unhealthy diet can lead to excess infant adiposity at birth. Specific dietary macro- and micronutrients have been shown to increase fat cell development in both in-vitro and in-vivo models and may therefore link maternal diet to increased infant adiposity. We hypothesized that high maternal dietary niacin intake during pregnancy, especially in combination with a high-fat diet (HFD) would increase infant adiposity. Methods We included 1040 participants from a pre-birth cohort of mother-infant pairs. Maternal diet was assessed using multiple 24-hour dietary recalls. HFD was defined as ≥30% of calories from fat and ≥12% of fat calories from saturated fat. Neonatal body composition (% fat mass [%FM], fat mass [FM], fat-free mass [FFM]) was measured by PEAPOD. We used multivariate regression to assess the joint effect of maternal dietary niacin and maternal HFD on neonatal body composition. Results Dietary niacin was not associated with neonatal body composition, and maternal HFD did not modify this finding. However, maternal HFD was independently associated with %FM (β = 0.8 [0.1, 1.4]%, p < 0.01] and FM (β = 32.4 [6.7, 58.0] g, p < 0.01).Conclusions for Practice Our results suggest that a HFD during pregnancy may increase infant adiposity, therefore supporting the need for improved diet counseling of pregnant women at both the clinical and community levels.