Fast Food Diet Research Articles

Blockade of 11β-hydroxysteroid dehydrogenase type 1 ameliorates metabolic dysfunction-associated steatotic liver disease and fibrosis

11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) is a key enzyme involved in the conversion of cortisone to active cortisol in the liver. Elevated cortisol levels can trigger oxidative stress, inflammation, and hepatocyte damage, highlighting the importance of 11β-HSD1 inhibition as a potential therapeutic approach. This study aimed to explore the effects of INU-101, an inhibitor of 11β-HSD1, on the development of metabolic dysfunction-associated steatotic liver disease (MASLD) and fibrosis. Our findings demonstrated that INU-101 effectively mitigated cortisol-induced lipid accumulation, reactive oxygen species generation, and hepatocyte apoptosis. Furthermore, 11β-HSD1 inhibition suppressed hepatic stellate cell activation by modulating β-catenin and phosphorylated SMAD2/3. INU-101 administration significantly reduced hepatic lipid accumulation and liver fibrosis in mice fed fast-food diet. This study suggests that INU-101 holds promise as a clinical candidate for treating MASLD and fibrosis, offering potential therapeutic benefits by targeting the intricate processes involving 11β-HSD1 and cortisol regulation in the liver.

Thermoneutrality Inhibits Thermogenic Markers and Exacerbates Nonalcoholic Fatty Liver Disease in Mice.

Nonalcoholic fatty liver disease (NAFLD) affects over a third of the US population and 25% globally, with current treatments proving ineffective. This study investigates whether manipulating brown adipose tissue (BAT) and beige fat activity by housing C57BL/6J mice at thermoneutral (27 °C) or standard temperatures (22 °C) impacts NAFLD development. Male mice were fed either a chow diet (CHD) or a "fast food" diet (FFD) for 10 weeks. Mice at 27 °C had reduced food intake but increased body weight and plasma leptin levels. FFD-fed mice at 27 °C had greater liver weight (2.6 vs. 1.8 g), triglyceride content (7.6 vs. 3.9 mg/g), and hepatic steatosis compared to those at 22 °C. Gene expression of fatty acid synthase, sterol regulatory element-binding protein 1, and fatty acid translocase CD36 was elevated in FFD-fed mice at 27 °C, but not in CHD-fed mice. Thermoneutral housing also reduced expression of thermogenic markers in BAT and inguinal white adipose tissue (WAT) and caused BAT whitening. In conclusion, thermoneutrality inhibits thermogenic markers and exacerbates NAFLD. Activating BAT or promoting WAT browning via cold exposure or other stimuli may offer a strategy for managing NAFLD.

The Role of Screening, Risk Factors, and Early Intervention in Preventing Diabetes in the Obese Population: A Systematic Review.

With its rising global prevalence, diabetes has become one of the most significant and challenging health problems afflicting the world's population today. The increasing burden of diabetes and its associated complications calls for immediate action for prevention which primarily includes addressing the risk factors.The most significant risk factor for the onset of diabetes is obesity. Obesity and diabetes rates have been rising simultaneously, posing a threat to patient mortality and driving up community healthcare costs. A weight loss of five percent or more of total body weight has been shown to improve the quality of life, reduce the need for pharmacological therapy for diabetes, and enhance glycemic control. This level of weight loss can have significant health benefits, particularly for individuals with diabetes or at risk for developing diabetes. We aim to conduct this systematic review to assess diverse risk factors contributing to the incidence of diabetes among the obese population and determine various preventive strategies and recommendations in practice for the prevention of diabetes in this cohort. As a result, we included original studies that recruited the obese and diabetic populations and defined preventive measures for early intervention. Additionally, we included studies published in the last 10 years (2014-2024) only for the latest evidence. Studies including obese populations with cardiovascular diseases and neurological disorders were excluded. The Newcastle-Ottoman Castle assessment tool was utilized to assess the quality of the studies. We included nine studies that recruited 60,645 patients and were published between 2015 and 2022. Findings suggest that obesity alone is a significant contributor to the occurrence or onset of diabetes. At the same time, the presence of other risk factors, including hypertension, dyslipidemia, elevated triglycerides, or HDL and LDL levels, may further increase the risk of diabetes and its associated complications among the obese population. Preventive strategies emphasize early intervention through increasing awareness and educating communities about risk factors and lifestyle interventions, including the limitations of fast food diets for the prevention of diabetes and weight control. Since obesity is considered to be an independent risk factor for the development of diabetes, addressing and managing it is of critical importance clinically. Targeted early interventions, including screening for risk factors, health promotion, and education activities, can aid in the adaptation of healthier lifestyles, which can reduce the burden of these diseases significantly.

Abstract P172: Potential Contribution of Social Factors in Reducing Population Disparities in Cardioprotective Health Behavior Between Bisexual, Gay/Lesbian, and Straight Adults

Background: Studies have demonstrated disparities in cardioprotective behavior by sexual orientation. Social factors have been associated with individual outcomes, but their impact on population disparities is unclear. We assessed if hypothetically intervening on social factors may reduce health behavior disparities by sexual orientation. Methods: We analyzed the intake survey data from the 2015-2023 Kaiser Permanente Research Bank. We compared unadjusted and demographics-standardized prevalence of selected health behaviors by sexual orientation (gay/lesbian or bisexual (LGB) vs straight adults (reference)). We then assessed the potential impact of hypothetically intervening on a single social factor (neighborhood safety, discrimination, education, income) on population disparities using a gap-closing estimand approach (i.e., modified inverse propensity weighting with g-computation). Results: We included 166,479 adults (mean age = 59 years), with 4.5% (7,476) gay/lesbian and 3% (4,936) bisexual. A higher proportion of LGB adults had documented current smoking, binge drinking, and low fruit intake compared to straight adults. Also, a higher proportion of bisexual adults had a high fast-food diet and inadequate sleep. Standardized prevalence of smoking, binge drinking, and inadequate sleep (bi only) remained higher in LGB adults. In gap-closing analysis, no change in gay/lesbian-straight disparities were observed. Reduction in bi-straight disparities in smoking (-2.5%, 95%CI: -3.5, -1.7) and sleep (-2.4%, 95%CI: -3.6, -1.1) may occur with higher college education rates. The sleep disparity (-2.4, 95%CI: -4.0, -0.93) may also decrease by reducing discrimination rates. None of the factors reduced the binge drinking disparity. (Table) Conclusion: LGB adults had higher prevalence of smoking, drinking, and inadequate sleep (bi only). Addressing single factors could reduce some LGB health behavior disparities but multi-factor interventions may be necessary to attain equity across orientations.

Hepatocyte-specific Epidermal Growth Factor Receptor Deletion Promotes Fibrosis but has no Effect on Steatosis in Fast-food Diet Model of Metabolic Dysfunction-associated Steatotic Liver Disease

Metabolic dysfunction-associated steatotic liver disease (MASLD) has become the most prevalent chronic liver disorder, with no approved treatment. Our previous work demonstrated the efficacy of a pan-ErbB inhibitor, Canertinib, in reducing steatosis and fibrosis in a murine fast-food diet (FFD) model of MASLD. The current study explores the effects of hepatocyte-specific ErbB1 (ie, epidermal growth factor receptor [EGFR]) deletion in the FFD model. EGFRflox/flox mice, treated with AAV8-TBG-CRE to delete EGFR specifically in hepatocytes (EGFR-KO), were fed either a chow-diet or FFD for 2 or 5 months. Hepatocyte-specific EGFR deletion reduced serum triglyceride levels but did not prevent steatosis. Surprisingly, hepatic fibrosis was increased in EGFR-KO mice in the long-term study, which correlated with activation of transforming growth factor-β/fibrosis signaling pathways. Further, nuclear levels of some of the major MASLD regulating transcription factors (SREBP1, PPARγ, PPARα, and HNF4α) were altered in FFD-fed EGFR-KO mice. Transcriptomic analysis revealed significant alteration of lipid metabolism pathways in EGFR-KO mice with changes in several relevant genes, including downregulation of fatty-acid synthase and induction of lipolysis gene, Pnpla2, without impacting overall steatosis. Interestingly, EGFR downstream signaling mediators, including AKT, remain activated in EGFR-KO mice, which correlated with increased activity pattern of other receptor tyrosine kinases, including ErbB3/MET, in transcriptomic analysis. Lastly, Canertinib treatment in EGFR-KO mice, which inhibits all ErbB receptors, successfully reduced steatosis, suggesting the compensatory roles of other ErbB receptors in supporting MASLD without EGFR. Hepatocyte-specific EGFR-KO did not impact steatosis, but enhanced fibrosis in the FFD model of MASLD. Gene networks associated with lipid metabolism were greatly altered inEGFR-KO, but phenotypic effects might be compensated by alternate signaling pathways.

Glabridin ameliorates intracellular events caused by palmitic acid and alcohol in mouse hepatocytes and fast food diet and alcohol -induced steatohepatitis and fibrosis in C57BL/6J mice model.

Steatohepatitis is a significant risk factor for end-stage liver disease. In this study, the therapeutic potential of Glabridin (GBD), an isoflavan derived from Glycyrrhiza glabra, is investigated in in-vitro and in-vivo models against palmitic acid (PA) or fast food (FF) diet+alcohol (EtOH). Mouse hepatocytes (AML-12cells) were treated with PA; 250μM+EtOH; 250μM±GBD (10μM and 25μM) for 24h. C57BL/6J mice fed with standard chow (SC) diet, fast food (FF) diet+intermittent oral ingestion of EtOH (10-50%v/v)±GBD (20mg/kg and 40mg/kg) for eight (8) weeks, were analyzed for histological features of steatohepatitis and fibrosis, biochemical indexes, and protein and gene expression studies related to oxidative stress, inflammation, lipogenesis, fibrosis, and apoptosis. GBD therapy considerably reduced intracellular events in AML-12cells exposed to PA+EtOH. GBD treatments significantly improved body metrics, biochemical indexes, and histological features in C57BL/6J mice compared to FF+EtOH. Moreover, protein and gene expression investigations revealed a strong therapeutic effects on oxidative stress, inflammation, steatosis, fibrosis, and apoptosis -related molecular signaling cascades. In conclusion, these findings suggest that GBD has a strong therapeutic potential to be developed as anti-steatohepatitis/fibrosis medicine.

Burgers, Fast Foods, and Increased Associated Risk for Atopic Dermatitis: A Cross-Sectional Study of Dietary Habits among Young Chinese Adults in Singapore/Malaysia

Background: We see increasing evidence that dietary and nutrients factors play a pivotal role in allergic diseases and recent global findings suggest that dietary habits influence the pathogenesis of atopic dermatitis (AD). Frequent consumption of fast food diets is associated with AD development. Despite the rising prevalence of AD in Asia, efforts in investigating the role of dietary habits and AD in adults are still lacking. Methods: We evaluated the association between the dietary intake of 16 food types and AD manifestations using our Singapore/Malaysia Cross-sectional Genetics Epidemiology Study (SMCGES) population. Dietary habits profiles of 11,494 young Chinese adults (1,550 AD cases/2,978 non-atopic controls/6,386 atopic controls) were assessed by an investigator-administered questionnaire. AD cases were further evaluated for their chronicity (550 chronic) and severity (628 moderate-to-severe). Additionally, we derived a novel food index, Quality of Diet based on Glycaemic Index Score (QDGIS), to examine the association between dietary intake of glycaemic index (GI) and various AD phenotypes. Results: The majority of AD subjects are distributed in the good (37.1%) and moderate (36.2%) QDGIS classes. From the multivariable analyses for age and gender, a moderate QDGIS class was significantly associated with a lower odds of AD (adjusted odds ratio (AOR): 0.844; 95% confidence interval (CI): 0.719–0.991; p < 0.05) and moderate-to-severe AD (AOR: 0.839; 95% CI: 0.714–0.985; p < 0.05). A good QDGIS class was only significantly associated with a lower odds of chronic AD (AOR: 0.769; 95% CI: 0.606–0.976; p < 0.05). Among high GI foods, frequent consumption of burgers/fast food was strongly associated with an increased risk of chronic and moderate-to-severe AD. Among low GI foods, increased intake frequencies of fruits, vegetables, and pulses decreased the odds of AD. Finally, we identified significant associations between frequent seafood, margarine, butter, and pasta consumption with an increased odds of AD despite them having little GI values. Conclusion: While genetic components are well-established in their risks associated with increased AD prevalence, there is still a lack of a focus epidemiology study associating dietary influence with AD. Based on the first allergic epidemiology study conducted here in Singapore and Malaysia, it laid the groundwork to guide potential dietary interventions from changing personal dietary habits.

A small animal model of NASH with progressive steatohepatitis -induced by fast food diet and alcohol in C57BL/6J mouse with high human pathophysiological proximity.

Non-alcoholic steatohepatitis (NASH) and alcoholic steatohepatitis (ASH) both can progress to end-stage liver disease (ESLD). No relevant animal models are available for studying the toxic consequences of concurrent fast food diet and alcohol usage in fibrosing NASH. As a result, dependable and short-term in-vivo models capable of recapitulating human disease pathophysiology are required for deciphering mechanistic insights and preclinical drug discovery programs. The current study aims to develop a mouse model for progressive steatohepatitis employing a fast food (FF) diet with intermittent oral alcohol (EtOH) administration. For eight (8) weeks, C57BL/6J mice were fed standard chow (SC) diet±EtOH or FF±EtOH. EtOH uses enhanced the histological characteristics of FF -induced steatohepatitis and fibrosis. A dysregulated molecular signaling cascade related to oxidative stress, steatosis, fibrosis, DNA damage, and apoptosis was evident at protein and gene expression levels in the FF+EtOH. The results from the in-vivo model were replicated in mouse hepatocyte cultures (AML-12) subjected to palmitic acid (PA)±EtOH exposures. The results of the present study indicate that the clinical hallmarks of human progressive steatohepatitis and fibrosis were achieved in our mice model, showing its suitability for preclinical research.

A Dietary Pattern for High Estimated Total Fat Amount Is Associated with Enhanced Allergy Sensitization and Atopic Diseases among Singapore/Malaysia Young Chinese Adults

Introduction: Frequent dietary patterns for fast food diets are suggested to be a risk factor for atopic disease development. Excessive dietary fats in fast foods are postulated to promote low-grade chronic inflammation. However, no studies in Asia have yet to characterize the dietary pattern for high-fat foods with atopic diseases. Thus, this study aims to assess the association between dietary fats with the prevalence of atopic diseases in an allergic cohort. Methods: Through an investigator-administered questionnaire that follows the International Study of Asthma and Allergies in Childhood (ISAAC) protocol, we evaluated the eating habits, lifestyle behaviours, sociodemographics, and atopic symptoms, and history among 11,494 young Chinese adults in Singapore and Malaysia. A skin prick test (SPT) for common house dust mites was also conducted to determine the atopic (allergic) status. We identified 1,550 atopic dermatitis (AD), 1,301 allergic asthma (AS), and 3,757 allergic rhinitis (AR) atopic cases. We derived a novel dietary index, Diet Quality based on Total Fat Amount (DQTFA), to examine the association between eating patterns for estimated total fat amount with various atopic outcomes. Results: There was a preponderance of subjects having positive SPT reaction (69.0%) with the prevalence of AR being the highest (32.7%), then AD (13.5%), and AS (11.3%). Additionally, there is a significantly higher proportion of subjects with an atopy background and atopic diseases consume diets with a high estimated mean fat amount. The adherence to a dietary pattern of the higher estimated total fat amount was shown to be strongly associated with all atopic diseases and exhibited dose-dependent responses in the univariate analysis. These associations remained significant even with the adjustments for age, gender, body mass index, use of alcohol, sedentary lifestyles, and physical activity. A dietary pattern for high-fat amount is more strongly associated with AS (adjusted odds ratio [AOR]: 1.524; 95% confidence interval [CI]: 1.216–1.725; p < 0.001) and AR (AOR: 1.294; 95% CI: 1.107–1.512; p < 0.001) compared to AD (AOR: 1.278; 95% CI: 1.049–1.559; p < 0.05). Finally, it was shown that having either one of the atopic comorbidities was strongly associated with a dietary pattern of high-fat amounts (AOR: 1.360; 95% CI: 1.161–1.594; p < 0.001). Conclusion: Our findings altogether provide initial evidence that the dietary pattern of a diet high in fat amount is associated with an increased risk of atopy and atopic diseases in young Chinese adults in Singapore and Malaysia. Balancing the consumption of dietary fats and changing personal dietary habits by choosing foods of the lower fat amount may reduce the associated odds of atopic diseases.

Relationship between knowledge and fast food with obesity in adolescents

Obesity is a risk factor of degenerative diseases which is a public health problem that covers almost the entire life cycle including adolescents. Consumption of fast food is suspected as one of the triggers of obesity in adolescents. Purpose: The purpose of this study was to find out the relationship of knowledge and fast food consumption with the incidence of obesity among adolescents in Kendari City, 2021. Method: A quantitative study with cross sectional design was conducted in December 2021 in the Kendari City area, Southeast Sulawesi. The results of the study: based on bivariate analysis showed that of 397 samples of good fast food diet as many as 151 people (38%) normal category and as many as 86 people (21.27%) who have a very good diet category normal and about 23 people (0.3%) have a diet that is not good category obesity. Based on bivariate analysis after conducting a statistical test with the Chi-Square test obtained p= =0,538&gt; 0.05 for knowledge and p = 0.007 &lt; 0.05 for fast food consumption. Conclusion: So it can be concluded that there was not relationship between knowledge with the incidence of obesity in adolescents and there was a significant relationship between fast food consumption with the incidence of obesity in adolescents.

Semaglutide Has Beneficial Effects on Non-Alcoholic Steatohepatitis in Ldlr-/-.Leiden Mice.

Semaglutide, a glucagon-like peptide-1 receptor agonist, is an antidiabetic medication that has recently been approved for the treatment of obesity as well. Semaglutide is postulated to be a promising candidate for the treatment of non-alcoholic steatohepatitis (NASH). Here, Ldlr-/-.Leiden mice received a fast-food diet (FFD) for 25 weeks, followed by another 12 weeks on FFD with daily subcutaneous injections of semaglutide or vehicle (control). Plasma parameters were evaluated, livers and hearts were examined, and hepatic transcriptome analysis was performed. In the liver, semaglutide significantly reduced macrovesicular steatosis (-74%, p < 0.001) and inflammation (-73%, p < 0.001) and completely abolished microvesicular steatosis (-100%, p < 0.001). Histological and biochemical assessment of hepatic fibrosis showed no significant effects of semaglutide. However, digital pathology revealed significant improvements in the degree of collagen fiber reticulation (-12%, p < 0.001). Semaglutide did not affect atherosclerosis relative to controls. Additionally, we compared the transcriptome profile of FFD-fed Ldlr-/-.Leiden mice with a human gene set that differentiates human NASH patients with severe fibrosis from those with mild fibrosis. In FFD-fed Ldlr-/-.Leiden control mice, this gene set was upregulated as well, while semaglutide predominantly reversed this gene expression. Using a translational model with advanced NASH, we demonstrated that semaglutide is a promising candidate with particular potential for the treatment of hepatic steatosis and inflammation, while for the reversal of advanced fibrosis, combinations with other NASH agents may be necessary.

Severe gestational diabetes mellitus in lean dams is associated with low IL-1α levels and affects the growth of the juvenile mouse offspring

We investigated how maternal gestational diabetes (GDM) impacts the metabolic status of offspring. GDM was induced in CD1 mice consuming a fast-food diet (FFD) by repeated low-dose streptozotocin injections before mating. Offspring of normoglycemic standard chow or the FFD consuming dams served as controls. In 4-week-old offspring weaned to standard chow, plasma concentrations of extracellular DNA, inflammatory markers, and parameters of the cardiometabolic status (glycemia, liver lipid content; body, organ, and fat weight) were determined. Two-factor analysis of variance indicated that the male offspring of GDM dams manifest postnatal growth retardation and lower relative kidney weight. Regardless of sex, GDM offspring manifest the lowest IL-1α levels, and other inflammatory markers showed mild and inconsistent alterations. Offspring of dams consuming the FFD displayed higher liver triacylglycerols content. The three groups of offspring showed no significant differences in glycemia and extracellular DNA. Partial least squares-discriminant analysis indicated that male GDM offspring present lower kidney, body, and brown adipose tissue weights; lower IL-1α levels, and higher concentrations of GM-CSF and IL-10 compared with their FFD counterparts. The model failed to select discriminative variables in females. In conclusion, in mice, maternal GDM in the absence of obesity adversely affects the early growth of juvenile male offspring.

Abstract A019: Cancer survivor-specific dietary patterns and risk of premature aging in adult survivors of childhood cancer: St. Jude Lifetime (SJLIFE) Cohort

Abstract Background: Childhood cancer survivors are a growing population at elevated risk for premature aging and age-related chronic health conditions (CHCs) compared to the general population. In the general population, diet affects many hallmarks of aging, including inflammation, metabolic dysfunctions, and molecular and epigenetic changes. We examined associations between dietary patterns and risk of premature aging in adult survivors of childhood cancer. Methods: Adult survivors (18-65 years old, mean [SD] age 31 [8.4] years) of childhood cancer enrolled in SJLIFE between 2007 and 2017 completed a 110-item food frequency questionnaire at enrollment (n=2,904). Sociodemographic, cancer, cancer treatments, and health history were abstracted from medical records; CHCs were clinically validated. Factor analysis was performed to identify dietary patterns specific to the study population. Premature aging was assessed using the Deficit Accumulation Index (DAI) based on 45 age-related CHCs and categorized into low (&amp;lt;0.2), medium (0.2-0.34), and high (&amp;gt;0.35) aging risk groups. Odds ratios (OR) and 95% confidence intervals (CI) were estimated using multinomial logistic regressions adjusting for potential confounders, such as sociodemographics, health behaviors, and cancer treatments. Individuals’ factor scores of each pattern were grouped into quintiles, and a median score of each quintile was entered as a continuous term in regression models. Results: 20% of survivors were at medium- and 8% were at high-risk for premature aging. Survivors at high-risk for premature aging were more likely to be female, smokers, have low socioeconomic status, and have received radiation therapy to head and neck, chest, spine, or abdomen compared to those at low premature aging risk. Three dietary patterns were identified: 1) plant-based, 2) fast-food, and 3) Western contemporary. A plant-based diet was characterized by greater intakes of vegetables, fruits, whole grains, and fish. A higher plant-based diet pattern score was associated with a lower risk of premature aging (OR=0.76, 95% CI: 0.62-0.94 for the high-risk group; OR=0.91, 95% CI: 0.79-1.04 for the medium-risk group). A fast-food diet was characterized by greater intakes of sweets, processed meat, refined grains, potato, high-fat dairy, and soda. A fast-food diet was related to a non-significant increased risk of premature aging (OR=1.20, 95% CI: 0.91-1.57 for the high-risk group; OR=1.18, 95% CI: 0.98-1.43 for the medium-risk group). A Western contemporary diet characterized by greater intakes of meat, pasta/rice, pizza, Mexican food, and fruit juice was associated with an increased risk of premature aging (OR=1.36, 95% CI: 1.05-1.78 for the high-risk group; OR=1.04, 95% CI: 0.87-1.26 for the medium-risk group). Conclusion: Our findings suggest that diet plays a role in aging, and a diet rich in plant-based foods may mitigate the risk of premature aging in childhood cancer survivors. Citation Format: Yikyung Park, Mei Wang, Tuo Lan, AnnaLynn M. Williams, Matthew J. Ehrhardt, Emily R. Finch, Jennifer Q. Lanctot, Shu Jiang, Kevin R. Krull, Gregory T. Armstrong, Melissa M. Hudson, Graham A. Colditz, Leslie Robison, Kirsten K. Ness. Cancer survivor-specific dietary patterns and risk of premature aging in adult survivors of childhood cancer: St. Jude Lifetime (SJLIFE) Cohort [abstract]. In: Proceedings of the AACR Special Conference: Aging and Cancer; 2022 Nov 17-20; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2022;83(2 Suppl_1):Abstract nr A019.

Survey-derived activity space-based exposures to fast food outlets and their cross-sectional associations with use of fast food outlets, diet quality and BMI.

There is a need for conceptual and methodological innovation in food environment-health research. We compared different operationalizations of survey-derived activity space exposures to fast food outlets (FFOs) in associations with use of FFO, diet quality and body mass index (BMI). FFO exposure was determined for home, work and a maximum of sixteen other locations reported by 1728 Dutch adults. Considerable differences in count of FFO between locations were found. Adjusted linear regression analyses resulted in small, unexpected associations with use of FFO, diet quality and BMI, whereby the strength of associations differed between exposure measures. Using home and work areas may be a cost-efficient compromise to capture large parts of the exposure to FFOs.

Estimation of nutritional status and prevalence of obesity in medical students – A descriptive study

Background: Obesity and malnutrition are common in adolescent and postadolescent age groups mainly due to their affinity for fast food and irregular diet. It was an effort to estimate the health status of students by conducting specific tests. Aim and Objectives: The objectives of this study were to estimate nutritional status and obesity in medical students. Materials and Methods: One hundred and eighteen medical students aged 17–22 years were included in the study. It was conducted between July 2017 and February 2018 in Veer Surendra Sai Institute of Medical Sciences and Research, Burla, India, after obtaining ethical clearance. Body mass index was calculated, and hemoglobin percentage was estimated for each student. The prevalence of underweight, overweight, obesity, and anemia was estimated. The findings were statistically analyzed. Results: The prevalence of obesity and malnutrition was calculated. Among them, 7.6% were underweight, 70.3% were normal, 20.33% were pre-obese, and 1.7% obese. Their nutritional status was correlated with food habits and physical activity. Conclusion: We can estimate the nutritional status and health status of students by performing simple procedures such as measurements of height and weight and estimation of hemoglobin. By this, we can make students aware of their health and improve their food habits by giving suggestions on their diet.

Comparison of dimension reduction methods for the identification of heart-healthy dietary patterns

Most nutritional epidemiology studies investigating diet-disease trends use unsupervised dimension reduction methods, like principal component regression (PCR) and sparse PCR (SPCR), to create dietary patterns. Supervised methods, such as partial least squares (PLS), sparse PLS (SPLS), and Lasso, offer the possibility of more concisely summarizing the foods most related to a disease. In this study we evaluate these five methods for interpretable reduction of food frequency questionnaire (FFQ) data when analyzing a univariate continuous cardiac-related outcome via a simulation study and data application. We also demonstrate that to control for covariates, various scientific premises require different adjustment approaches when using PLS. To emulate food groups, we generated blocks of normally distributed predictors with varying intra-block covariances; only nine of 24 predictors contributed to the normal response. When block covariances were informed by FFQ data, the only methods that performed variable selection were Lasso and SPLS, which selected two and four irrelevant variables, respectively. SPLS had the lowest prediction error, and both PLS-based methods constructed four patterns, while PCR and SPCR created 24 patterns. These methods were applied to 120 FFQ variables and baseline body mass index (BMI) from the Multi-Ethnic Study of Atherosclerosis, which includes 6814 participants aged 45-84, and we adjusted for age, gender, race/ethnicity, exercise, and total energy intake. From 120 variables, PCR created 17 BMI-related patterns and PLS selected one pattern; SPLS only used five variables to create two patterns. All methods exhibited similar predictive performance. Specifically, SPLS’s first pattern highlighted hamburger and diet soda intake (positive associations with BMI), reflecting a fast food diet. By selecting fewer patterns and foods, SPLS can create interpretable dietary patterns while maintaining predictive ability.

A longitudinal investigation of a fast-food diet and alcohol-induced chronic liver damage in a novel murine model that reflects clinical disease progression

A longitudinal investigation of a fast-food diet and alcohol-induced chronic liver damage in a novel murine model that reflects clinical disease progression

(Pro)renin receptor inhibition attenuated liver steatosis, inflammation, and fibrosis in mice with steatohepatitis.

The (Pro)renin receptor (PRR) is reportedly involved in hepatic lipid metabolism and hepatocyte PRR knockdown protects mice against hepatosteatosis. However, the impact of PRR inhibition on liver inflammation and fibrosis in nonalcoholic steatohepatitis (NASH) remains unclear. Herein, C57BL/6 mice were fed a normal chow diet or fast food diet (FFD) for 24 weeks. Lentivirus-mediated PRR short hairpin RNA (shRNA) or handle region peptide (HRP), a PRR blocker, was administered for PRR inhibition. Mouse primary hepatocytes were cultured with palmitic acid, prorenin, siRNA-targeted PRR, and HRP. In FFD-fed mice, PRR inhibition via lentivirus-mediated PRR knockdown or HRP significantly attenuated liver steatosis, inflammation, and fibrosis. Mechanistically, PRR knockdown or HRP decreased hepatic acetyl-CoA carboxylase (ACC) abundance and upregulated peroxisome proliferator-activated receptor-alpha (PPARα). HRP treatment also decreased hepatic PRR expression. In addition, intrahepatic oxidative stress, apoptosis and inflammatory cell recruitment were ameliorated by PRR knockdown or HRP treatment, along with suppression of proinflammatory cytokine expression. PRR inhibition downregulated the hepatic expression of profibrotic factors, as well as TGF-β1/SMAD3 pathway. In primary mouse hepatocytes, PRR knockdown with siRNA or HRP downregulated cellular ACC and increased PPARα expression. In conclusion, our findings revealed that PRR inhibition attenuated hepatic steatosis, inflammation, and fibrosis in mice with NASH. Accordingly, targeting PRR signaling may serve as a potential treatment for NASH.

Empagliflozin in mice fed on a fast-food diet: Preliminary biochemical data

Aim: Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease affecting a large proportion of the general population (25%). The aim of this study was to evaluate the effect of a sodium-glucose co-transporter 2 inhibitor, empagliflozin, on NAFLD and the preliminary data of week 8 are hereby presented. Material and methods: Twenty-four C57Bl/6 mice of both genders were randomly assigned in three groups: 8 mice fed on chow diet (control group), 8 mice fed fast-food diet (FFD) and empagliflozin, and 8 mice fed FFD without empagliflozin for 8 weeks. Weight measurement, and blood sampling for the measurement of glucose, alanine aminotransferase, total cholesterol and triglycerides were performed at baseline and week 8. Results: Between-group comparisons did not show significant differences between FFD groups with and without empagliflozin. The only between-group difference regarding empagliflozin group was in cholesterol at week 8, which was higher compared to control group (p=0.009). Within-group comparisons showed increases in total cholesterol in both FFD groups, ALT in FFD/empagliflozin group and glucose in FFD group. Despite the expected increase in body weight, no biochemical change was observed in the control group. Conclusions: Empagliflozin did not show preventive benefits on body weight or metabolic biochemical parameters after 8 weeks of treating FFD mice, thus, possibly highlighting that 8 weeks may be short period for FFD to exert its adverse effects in full, as well as for empagliflozin to exert any potentially beneficial effect.

A comparative study on roles of natural killer T cells in two diet-induced non-alcoholic steatohepatitis-related fibrosis in mice

Background Immune responses are important in the progression of non-alcoholic fatty liver disease (NAFLD). Natural killer T (NKT) cells are main components of the innate immune system that modulate immunity. However, the role of NKT cells in NAFLD remains controversial. Objective We aimed to investigate the role of NKT cells in non-alcoholic steatohepatitis (NASH)-related fibrosis in fast food diet (FFD)- and methionine choline-deficient (MCD) diet-induced mouse models. Methods Hepatic NKT cells were analysed in wild-type (WT) and CD1d-/- mice fed FFD or MCD diets. Hepatic pathology, cytokine profiles and liver fibrosis were evaluated. Furthermore, the effect of chronic administration of α-galactosylceramide (α-GalCer) on liver fibrosis was investigated in both FFD- and MCD-treated mice. Results FFD induced a significant depletion of hepatic NKT cells, thus leading to mild to moderate NASH and early-stage fibrosis, while mice fed MCD diets developed severe liver inflammation and progressive fibrosis without a significant change in hepatic NKT cell abundance. FFD induced a similar liver fibrogenic response in CD1d-/- and WT mice, while MCD induced a higher hepatic mRNA expression of Col1α1 and TIMP1 as well as relative fibrosis density in CD1d-/- mice than WT mice (31.8 vs. 16.3, p = .039; 40.0 vs. 22.6, p = .019; 2.24 vs. 1.59, p = .036). Chronic administration of α-GalCer induced a higher hepatic mRNA expression of TIMP1 in MCD-treated mice than controls (36.7 vs. 14.9, p = .005). Conclusion NKT cells have protective roles in NAFLD as the disease progresses. During diet-induced steatosis, mild to moderate NASH and the early stage of fibrosis, hepatic NKT cells are relatively depleted, leading to a proinflammatory status. In severe NASH and the advanced stage of liver fibrosis, NKT cells play a role in inhibiting the NASH-related fibrogenic response. Chronic administration of α-GalCer induces NKT cell anergy and tolerance, which may play a role in promoting the liver fibrogenic response.