Thursday, 31 October 2013

Obesity and Type II Diabetes

Obesity is defined as a medical condition of excess body fat has accumulated overtime, while overweight is a condition of excess body weight relatively to the height. According to the Body Mass Index(BMI), a BMI between 25 to 29.9 is considered over weight, while a BMI of over 30 is an indication of obesity. According to the statistic, 68% of American population are either overweight or obese.

Type II diabetes
Diabetes is defined as a medical condition of insufficient insulin entering the bloodstream to regulate the glucose. It is either caused by cells in the pancreas dying off or receptor sites clogged up by the accumulation of fat and cholesterol. In some case, diabetes is also caused by allergy reactions of cells in our body.

How do calculate your BMI index
BMI= weight (kg)/ height (m2)

How obesity cause type II diabetes
Type II diabetes is a result of insulin resistance and obesity
is considered as a risk factor for developing insulin resistance.
1. According to the article of "Obesity and insulin resistance" by Barbara B. Kahn and Jeffrey S. Flier (1), researchers indicated that the association of obesity with type 2 diabetes has been recognized for decades, and the major basis for this link is the ability of obesity to engender insulin resistance. Insulin resistance is a fundamental aspect of the etiology of type 2 diabetes and is also linked to a wide array of other pathophysiologic sequelae including hypertension, hyperlipidemia, atherosclerosis (i.e., the metabolic syndrome, or syndrome X), and polycystic ovarian disease.
In conclusion, the author wrote that advances over the last decade have expanded our understanding of the role of adipocytes in biology, and this has begun to provide mechanistic insights into the causal relationship between obesity and diabetes. It is now clear that adipocytes function as endocrine glands with wide-reaching effects on other organs including the brain. The release of a wide variety of molecules including hormones such as leptin, cytokines such as TNF-α, and substrates such as FFAs allows the adipose organ to play a major regulatory role in energy balance and glucose homeostasis.

2. Adipogenesis
Some researchers suggested that adipogenesis may be the cause of obesity and insulin resistance due to preadipocytes become adipocytes ( lipocytes and fat cells) as a result of gene expression. According to the study of "Obesity, adipogenesis and insulin resistance." [Article in English, Spanish] by Ros Pérez M, Medina-Gómez G. (Source from Departamento de Bioquímica, Fisiología y Genética Molecular, Universidad Rey Juan Carlos, Facultad de Ciencias de la Salud, Alcorcón, Madrid, España.), posted in PubMed, researchers found that Obesity is considered as a risk factor for developing insulin resistance. Increased adipose tissue has been related to an increased production of pro-inflammatory cytokines which, together with fatty acids, appear to be responsible for the development of insulin resistance. Thus, a greater or lesser expansibility or ability of adipose tissue to store lipids also appears to play a significant role in the development of insulin resistance because overcoming of this capacity, which is variable in each case, would result in leaking of lipids to other tissues where they could interfere with insulin signaling.

3. Etc.

1. Can Gene and Inherited factor cause of Obesity and type II diabetes be changed
Obesity and type II diabetes as a result of genetic susceptible or heredity can be prevented, according to the study of " Lifestyle and Genetics in Obesity and type 2 Diabetes." by Temelkova-Kurktschiev T, Stefanov T. (Source from Medicobiological Unit.) posted in PubMed, researchers found that gene-lifestyle interaction studies suggest that
a. Genetic susceptibility to obesity and type 2 diabetes may be partially or totally kept under control by healthy lifestyle or lifestyle modification and that lifestyle determines whether an individual is likely to develop the disease.
b. Inherited factors, however, seem to influence individual response to a lifestyle intervention program and even the motivation for lifestyle change. Personalized interventions according to genotype may be, therefore, considered in the future.
By then lifestyle modification targeting dietary change and increased physical activity may be recommended for successful obesity and type 2 diabetes prevention irrespectively of genetic susceptibility.

2. Leptin and Obesity and Type 2 Diabetes
Since leptin is the protein product of the obese gene, many researchers have tries to develop the mew approach to treat obesity and type 2 diabetes. In a study of " Novel Approaches to the Treatment of Obesity and Type 2 Diabetes Mellitus: Bioactive Leptin-Related Synthetic Peptide Analogs." by Grasso P. (Source from Department of Medicine, Division of Endocrinology and Metabolism Albany Medical College, MC 141, Albany, NY 12208, USA., posted in PubMed, researches indicated that The pleiotropic nature of leptin has been confirmed by demonstration of a role for leptin in hematopoiesis, angiogenesis, immune function, osteogenesis, reproduction, and wound healing. Unfortunately, the results of the majority of clinical trials with recombinant human leptin indicated that its effectiveness in restoring energy balance and correcting obesity-related endocrinopathies in genetically obese rodent models extended only to the management of those rare forms of human obesity caused by mutation in the ob gene. Failure of leptin in the clinic, and withdrawal of fenfluramine, phentermine, and sibutrimine from clinical use in the United States, have stimulated new approaches in the development of anti-obesity and anti-diabetes pharmacophores.

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(1) Division of Endocrinology and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USAAddress correspondence to: Barbara B. Kahn, Division of Endocrinology and Metabolism, Beth Israel Deaconess Medical Center, 99 Brookline Avenue, Boston, Massachusetts 02215, USA. Phone: (617) 667-5422; Fax: (617) 667-2927; E-mail: The Journal of Clinical investigation

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