Obesity Is A Rising Epidemic Throughout The United States Of America

Being overweight, eating poorly, and not exercising are becoming an epidemic in America, especially among college students. Most of the research on it states the same things, however the first research article I found speaks more to the behavior and its current affects on college students’ health. A slew of doctors and Jesse S. Morrell wrote an article about “Risk Factors Among College Men and Women” in relationship to obesity. The opening of this article stated that “an estimated 300,000 deaths each year are attributable to obesity… and young adults have experienced dramatic increases in obesity rates,” (Morrell, 2012, pg. 82). This statistic is what really got the research going and helped the researchers focus specifically on college-aged individuals. Upon diving into their research, the authors found more alarming statistics and related diseases. This included a recognizable relationship between obesity in young people and chronic disease risk, especially diabetes and cardiovascular disease (Morrell, 2012, pg. 82). In fact, CVD was the second leading cause of death in the US in that college-age group showing that our generation is at a greater risk for health problems than ever before due to our lack of exercise and healthy diets. Researchers then took to college campuses to examine students and their habits and provide risk assessments to promote healthier lifestyles and hopefully decrease the probability of CVD and DM through the metabolic syndrome system,

The United States of America is the fattest country in the world. Obesity in America has reach epidemic proportions. Obesity and weight gain has become major concern of public health in the United States. In every state, at least twenty percent of adults are obese, and in twelve of these states the obesity rate is above thirty percent. Mississippi currently holds the highest rate of obesity with 34.9 percent of its residents being obese. On the contrary, Colorado has the lowest rate of obesity with 20.7 percent. CNN estimated that annual medical care costs due to obesity reached $147 billion, but the Institute of Medicine estimates it is closer to $190 billion.

In wild type mouse there is no effect on food intake, body weight and blood glucose though we give more leptin because here the leptin receptors are constant. But, in ob/ob mouse the food intake, body weight and blood glucose levels are decrease because the presence of leptin receptor. However, in the db/db mouse there is no effect due to the absence of the leptin

In correlation with weight gain, HFCS significantly increases the rate of type II diabetes in the United States. Diabetes occurs when there is an insufficient amount of insulin to transport glucose to body cells to be used as fuel. As a result of this, the cells starve, causing the degeneration of tissues and organs. HFCS increases the likelihood of diabetes because the obesity caused by HFCS consumption vastly contributes to the inability of

This explained the low birth weight in undernourished rats but was rejected by Hardikar when he analysed potential single nucleotide polymorphism loci including methylenetetrahydrofolate reductase (mthfr) and discovered no genetic alterations. The thrifty genotype model also suggests an undernourished intrauterine environment is responsible for fetal programming that increases susceptibility to type - 2 diabetes in offspring. The second generation of recuperation rats should have demonstrated less susceptibility to type - 2 diabetes as they were well nourished during fetal development, but Hardikar discovered the undernourished and recuperation rats both demonstrated an increased susceptibility to streptozotocin induced diabetes that indicates type - 2 diabetes was not explained by low intrauterine

(TIE) and (CSE) treatment prevented the increase in fasting serum insulin, TG, TC, VLDL, and LDL when comparing with the F group. Fructose feeding led to a decrease in fasting serum DHEAS, and HDL levels in the F group compared with the control. TIE and CSE treatment prevented the decrease in fasting serum DHEAS, and HDL

Al Rabey et al., (2013) analyzed that twenty male Albino rats were divided into four groups each consisted of five rats and fed the specified test diets for eight weeks. The first group (G1) is the negative group which was fed basal diet, the second group (G2) was fed 1.0% cholesterol, was the third group (G3) fed 1.0% cholesterol and 10% oats bran, and the fourth group (G4) was fed 1.0% cholesterol and 10% barley bran. Feeding rats on 1% cholesterol significantly increased serum total cholesterol, low density lipoprotein, and very low density lipoprotein and triglyceride and decreased serum high density lipoprotein. Hypercholesterolemic rats supplemented with oat bran and barley bran showed significant decrease in lipid parameters, significant increase in high density lipoprotein-cholesterol, improved antioxidant enzyme, and improved histopathology of kidney, liver, heart, and testes. Oat bran appeared more efficient than barley bran in lowering the lipid profile levels in hypercholesterolemic rats [55].

Randomized-control trials and cohort studies were identified by searching PubMED and some were provided by Vifor (financial supporter for the study). Studies were then rated on a scale of 1-5, with 5 equaling the lowest potential for bias. Studies with a score of two or greater were included in the study to limit bias. Patients in these studies were given either IV ferric carboxymaltose (n=2,348), IV iron sucrose (n=384), oral iron (n=832), or placebo (n=762). Results showed IV ferric carboxymaltose was better at attaining the target hemoglobin increase than comparators (NNT = 6.8; 95% CI: 5.3-9.7). Results also showed IV ferric carboxymaltose was better at reaching the target hemoglobin levels (NNT=5.9; 95% CI: 4.7-8.1). This meta-analysis was missing some hallmarks of a well-constructed meta-analysis (a stated question to answer, an explicitly-stated search strategy and evidence table). This qualifies as a large limitation to the

Hemochromatosis is an inherited recessive genetic disorder where the body absorbs and stores too much iron in the body. Often when iron is discussed in United States diets it is to combat the portion of our society that is anemic due to and iron-deficient diet, but we often fail to think about the other end of the spectrum. Unlike people with iron-deficiently anemia individuals with hemochromatosis have an excessive amount of iron in their body which can lead to overtime organ damage. “If hemochromatosis is not detected and treated early, it may eventually cause serious irreversible disorders such as arthritis, liver disease, heart disease and diabetes later in life.”1 Unfortunately there are few symptoms of the disease, and of those symptoms they are very generic like chronic fatigue, weakness, joint pain, depression, shortness of breath. As you can see those physical symptom can easily point to many different issues (including iron-deficient anemia) before a doctor will usually think about hemochromatosis. Hemochromatosis vague beginning symptoms are usually why is so underdiagnosed by doctors in the early stages. Thus many times hemochromatosis is not diagnosed until the progression

Obesity related insulin resistance is a common metabolic disease and has been found to occur due to alterations in the genetic constitution of an individual or in the environmental conditions.

Male and female proximal-tubule select IR/IGF double KO mice were bred and genotyped at Georgetown University. The mice were fed control or a high-fructose diet for 4 weeks. The mice were euthanized humanely and kidneys were collected for analysis. Western blots were completed on whole kidney homogenates to assess the expression of Napi-2, KHK, GLUT5, IR, IGFR and NHE3. Electrolyte levels were measured in urine and plasma using EasyLyte electrolyte analyzer. We found that across both sexes, the expression of GLUT5 and was increased in fructose diet in both WT and KO

The micronutrient iron is crucial for life; however, maintenance of iron homoeostasis is critical since its deficiency or excess both leads to a pathological condition. Unlike like other nutrients, the iron homoeostasis is regulated at the level of absorption in the intestine and not via excretion. When the body iron store declines or when there is an increase in demand, the iron homoeostasis is maintained by the increase in absorption and vice versa. The recent biomedical advance has witnessed the hormone produced by liver, hepcidin as a prime regulator of iron homoeostasis by inhibiting iron absorption; however, the regulation of the hepcidin expression is complex and multifactorial. In this review, we explored and compared the recent advances in understanding the regulation of hepcidin expression.

High-fat diet (HFD) in combination with low-dose Streptozotocin (STZ) model proves to be better choice to induce type 2 diabetes (Zhang et al., 2008). The HFD-fed rats show significant increase in basal plasma

The serum MDA level was increased in high-fat control group, compared to the normal control group , due to increase in fatty acids and decrease in serum antioxidant capacity. Singh et al. reported that the use of pioglitazone (30 mg / kg), has reduced the serum MDA levels (19). Consistently, in the present study, the serum MDA levels in the pioglitazone group was significantly decreased, compared to the control group (p <0.05). In a study by Hussian and colleagues, pioglitazone has reduced the serum glucose, LDL and cholesterol level in non-diabetic hyperlipidemia rats, compared to the controls (20). In the current study, serum glucose, LDL and serum cholesterol levels were decreased in the third group, compared to the second group (p <0.05). The UCP-1 gene expression alterations observed in this study, can be due to the lipid alterations in the high fat diet groups The UCP-1 gene expression alterations observed in this study, can be due to the high fat consumption in these groups.

44 Inverse association between serum vitamin D and glucose levels, 38,39,45 and insulin resistance 20,38,39,46-48 have been established in several epidemiological