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

2012 ◽  
Vol 19 (3) ◽  
pp. 273-283
Author(s):  
Maria Niţescu ◽  
Adrian Streinu-Cercel ◽  
Marina Oţelea ◽  
Florentina Ligia Furtunescu
Keyword(s):  
Metabolic Syndrome ◽  
Medical Students ◽  
Food Intake ◽  
Junk Food ◽  
Nutritional Behavior ◽  
The 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:

The effect of high multivitamin diet during pregnancy on food intake and glucose metabolism in Wistar rat offspring fed low-vitamin diets post weaning

2011 ◽  
Vol 2 (5) ◽  
pp. 302-310 ◽  
Author(s):  
I. M. Y. Szeto ◽  
P. S. P. Huot ◽  
S. A. Reza-López ◽  
A. Jahan-mihan ◽  
G. H. Anderson
Keyword(s):  
Metabolic Syndrome ◽  
Food Intake ◽  
Insulin Response ◽  
Fold Increase ◽  
Wistar Rat ◽  
Oral Glucose ◽  
Glucose Response ◽  
Rat Offspring ◽  
Vitamin Content ◽  
The Metabolic Syndrome

Rat offspring born to dams fed a high multivitamin diet (HV) are shown to have increased risks of obesity and metabolic syndrome. We hypothesized that a low-vitamin postweaning diet would enhance these characteristics in offspring born to HV dams. During pregnancy, Wistar rats were fed the AIN-93G diet with or without a 10-fold increase in vitamin content. In Experiment 1, at weaning, males were fed the recommended diet (RV) or a diet with 1/3 the vitamin content (1/3 RV) for 12 weeks. In Experiment 2, males and females were fed the RV diet or 1/6 RV diet for 35 weeks. Body weight was measured on a weekly basis, food intake on a daily basis, and for 1 h after an overnight fast following glucose gavage at 6, 12 and 24 weeks. Blood glucose and insulin responses to an oral glucose load were measured at 30 weeks. Males from HV dams, compared with those from RV dams, gained more weight in Experiment 1 (+7%,P< 0.05) and Experiment 2 (+11%,P< 0.0001), along with higher glucose response (+33%,P< 0.05). The 1/6 RV pup diet led to lower weight gain in males (−16%,P< 0.0001) and females (−13%,P< 0.0005), and lower food intake in males (−9%,P< 0.01) independent of the gestational diet. Females on the 1/6 RV diet and from HV dams had higher 1 h food intake (+36%,P< 0.05) and lower insulin response (−25%,P< 0.05) compared with those from RV dams. Exposure of the offspring to low-vitamin diets did not amplify the expression of the metabolic syndrome observed in those born to dams fed an HV diet.

Generation and characterization of two novel mouse models exhibiting the phenotypes of the metabolic syndrome: Apob48−/−Lepob/ob mice devoid of ApoE or Ldlr

2008 ◽  
Vol 294 (3) ◽  
pp. E496-E505 ◽  
Author(s):  
David J. Lloyd ◽  
Jocelyn McCormick ◽  
Joan Helmering ◽  
Ki Won Kim ◽  
Minghan Wang ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Food Intake ◽  
Apolipoprotein B ◽  
Plasma Cholesterol ◽  
Density Lipoprotein ◽  
Suppressive Effect ◽  
Human Condition ◽  
Atherogenic Dyslipidemia ◽  
Direct Role ◽  
The Metabolic Syndrome

The metabolic syndrome is a group of disorders including obesity, insulin resistance, atherogenic dyslipidemia, hyperglycemia, and hypertension. To date, few animal models have been described to recapitulate the phenotypes of the syndrome. In this study, we generated and characterized two lines of triple-knockout mice that are deficient in either apolipoprotein E (Apoe−/−) or low-density lipoprotein receptor (Ldlr−/−) and express no leptin (Lepob/ob) or apolipoprotein B-48 but exclusively apolipoprotein B-100 (Apob100/100). These two lines are referred to as Apoe triple-knockout-Apoe 3KO (Apoe−/−Apob100/100Lepob/ob) and Ldlr triple-knockout-Ldlr 3KO (Ldlr−/−Apob100/100Lepob/ob) mice. Both lines develop obesity, hyperinsulinemia, hyperlipidemia, hypertension, and atherosclerosis. However, only Apoe 3KO mice are hyperglycemic and glucose intolerant and are more obese than Ldlr 3KO mice. To evaluate the utility of these lines as pharmacological models, we treated both with leptin and found that leptin therapy ameliorated most metabolic derangements. Leptin was more effective in improving glucose tolerance in Ldlr 3KO than Apoe 3KO animals. The reduction of plasma cholesterol by leptin in Ldlr 3KO mice can be accounted for by its suppressive effect on food intake. However, in Apoe 3KO mice, leptin further reduced plasma cholesterol independently of its effect on food intake, and this improvement correlated with a smaller plaque lesion area. These effects suggest a direct role of leptin in modulating VLDL levels and, likewise, the lesion areas in VLDL-enriched animals. These two lines of mice represent new models with features of the metabolic syndrome and will be useful in testing therapies targeted for combating the human condition.

scholarly journals A study on the prevalence of obesity and metabolic syndrome among students of a medical college

2017 ◽  
Vol 5 (6) ◽  
pp. 2331
Author(s):  
Srinivas G. N. S. V Kandula ◽  
Sasi Sekhar T. V. D. ◽  
Shruti Kongara ◽  
Santhosh Kumar Arepalli
Keyword(s):  
Metabolic Syndrome ◽  
Medical Students ◽  
Waist Circumference ◽  
International Diabetes Federation ◽  
Strong Relationship ◽  
Cross Sectional Study ◽  
Individual Risk ◽  
Junk Food ◽  
Cross Sectional ◽  
Prevalence Of Obesity

Background: Obesity is emerging as a serious problem throughout the world. The overall life expectancy is significantly shortened and the quality of life decreased in those who are excessively overweight. Metabolic syndrome (MetS) is characterized by a constellation of individual risk factors of cardiovascular disease. Central obesity is a key feature of this syndrome, reflecting the fact that the syndrome’s prevalence is driven by strong relationship between waist circumference and increasing obesity. Awareness about MetS in medical students is the need of the hour.Methods: This cross-sectional study was conducted at Dr. PSIMS and RF, Chinnoutpalli, Andhra Pradesh, India involving 400 medical students. A pre-tested questionnaire, measurement of blood pressure, fasting glucose level, fasting lipid profile, anthropometric variables such as height, weight, waist circumference and hip circumference were taken. Metabolic syndrome was defined based on the International Diabetes Federation criteria. Data was processed using SPSS version 16. T-test, chi-square test, fisher’s exact test, anova and odd’s ratio were used for statistical analysis.Results: 59% of the study population was female. The prevalence of obesity was 4%, with majority being males (81.25%) The MetS prevalence as per the International diabetes federation (IDF) criteria was 6% (n=24). The prevalence of MetS in males was 12.19% (n=20) and in females 1.69%. (n=4). The risk of developing metabolic syndrome is high among those who smoke, consume alcohol, consume junk food and sleep for longer durations.Conclusions: The prevalence of metabolic syndrome is 6%. A significant association is established between life style habits like smoking, alcohol consumption, junk food consumption, sleep duration and MetS.

scholarly journals Orectic And Anorectic Peptides And Their Implication In Obesity And The Metabolic Syndrome

2015 ◽  
Vol 22 (2) ◽  
pp. 187-191
Author(s):  
Alina Bodea ◽  
Amorin Remus Popa
Keyword(s):  
Metabolic Syndrome ◽  
Food Intake ◽  
Energy Expenditure ◽  
Neuropeptide Y ◽  
Related Protein ◽  
The Metabolic Syndrome ◽  
Hypothalamic Neuropeptides ◽  
Clinical Conditions ◽  
Agouti Related Protein ◽  
Adipose Cells

AbstractBackground and aims: Cardiovascular diseases, diabetes mellitus, the metabolic syndrome and obesity are now globally widespread clinical conditions, addressing different ages, lately extending to young and children. The causes are multiple, involving an interaction between individual genetic risk factors and environmental factors. Many studies showed the importance of the hypothalamic neuropeptides and other neuropeptides in the regulation of the balance between food intake and energy consumption. We reviewed 25 recent research studies describing the physiological and physiopathological mechanisms of the orectic and anorectic peptides and their interaction to adjust the balance between food intake and energy expenditure.Conclusions: The hypothalamus, through its nuclei (arcuate and paraventricular) controls the balance between food intake and energy expenditure. The proopiomelanocortin (POMC) / Cocaine and amphetamine-related transcript (CART) neurons represent the anorectic centre. The neurons that release neuropeptide Y (NPY) and agouti-related protein (AgRP) by stimulation form the orectic centre. The neuropeptide Y (NPY) is the main hypothalamic orectic neuropeptide. Its action, besides stimulating the orectic effect, is to modulate the release of other hypothalamic orectic and anorectic neuropeptides. In addition, the energy balance is regulated by adipokines released by the adipose cells, hormones and neurotransmitters, blood glucose level and other metabolites.

scholarly journals A genetic variant of the NAMPT gene rs4730153 as a risk factor for the metabolic syndrome in younger age: a single-centre pilot study in Yogyakarta, Indonesia

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Anggelia Puspasari ◽  
Pramudji Hastuti ◽  
Ahmad Hamim Sadewa ◽  
Rosdiana Mus ◽  
Citra Maharani ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Food Intake ◽  
Cardiometabolic Risk ◽  
Genetic Variant ◽  
Allele Carrier ◽  
Metabolic Risk ◽  
Single Centre ◽  
The Metabolic Syndrome ◽  
Younger Age ◽  
Nicotinamide Phosphoribosyl Transferase

Abstract Background The genetic variation of nicotinamide phosphoribosyl transferase (NAMPT) gene rs4730153 is reported to be associated with cardiometabolic risk, but the results are inconsistent between populations. Ethnicity, metabolic risk and lifestyle play a role in the association of the genetic variant and the metabolic syndrome (MetS). To the best of our knowledge, no research has yet been published concerning the Javanese population, so this study aimed to investigate the association of rs4730153 with MetS and its interaction with metabolic risk and lifestyle. Results The GG genotype (p = 0.031; OR 95% CI 3.88 [1.13–13.33]), GA+GG genotype (p = 0.048; OR 95% CI 10.52 [1.02–108.01]) and G allele carrier (p = 0.006; OR 95% CI 4.19 [1.51–11.64]) of rs4730153 had a higher risk of the MetS after adjusting for obesity, hypercholesterolemia, smoking and food intake. The risk was statistically significant for the younger age group ≤ 45 years old. Conclusion The GG, GA+GG genotype and G allele carrier of rs4730153 have a higher risk of the MetS, especially those who are obese, hypercholesterolemic and smokers and have a higher food intake in those aged ≤ 45 years old. Further larger, multicentre studies are required to confirm these pilot results.

scholarly journals Diet, diabetes and schizophrenia: Review and hypothesis

2004 ◽  
Vol 184 (S47) ◽  
pp. s102-s105 ◽  
Author(s):  
Malcolm Peet
Keyword(s):  
Risk Factors ◽  
Metabolic Syndrome ◽  
Food Intake ◽  
General Population ◽  
Lifestyle Factors ◽  
Lifestyle Interventions ◽  
Common Pathway ◽  
Nutritional Factors ◽  
The Metabolic Syndrome

BackgroundDiabetes is more common in people with schizophrenia than in the general population.AimsTo explore the possible reasons for the association between diabetes and schizophrenia.MethodDiet and other lifestyle factors in patients with schizophrenia were reviewed as risk factors for diabetes.ResultsPeople with schizophrenia show features of the metabolic syndrome at the onset of illness, before treatment. They also eat a poor diet, take little exercise and have high rates of smoking. Food intake may be increased further by antipsychotic medication. Nutritional factors appear to have a key role in the development of diabetes in patients with schizophrenia and may also affect the outcome and severity of schizophrenia. A common pathway through which diet might contribute to the development of both diabetes and schizophrenia is proposed.ConclusionsLifestyle factors may influence outcomes in both diabetes and schizophrenia. Lifestyle interventions are the key to improving the long-term health of people with schizophrenia.

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