Obesity etiology

The etiology of obesity is usually unknown, but it is likely multifactorial and related to varying contributions from genetic, environmental, and physiologic factors. 

Osteoarthritis proves to be a more complex disease than autoimmune disease, with multiple variable manifestations like knee, hip, hand, DIP, elbow, shoulder, and spinal joints OA, which have different risk factors. The etiology of OA is multifactorial with inflammatory, metabolic and mechanical causes. A number of personal and environmental risk factors, such as obesity, occupation, and trauma, may initiate various pathological pathways. OA comprises degeneration of articular cartilage together with changes in subchondral bone of the joint margins and mild intraarticular inflammation. 

Except for one case/° recent clinically oriented MRS studies of human liver have been at 1.5T. Several studies applied in vivo MRS to diffuse liver disease. ° °" The PDE intensity was lower in cirrhosis than in controls ° and served to distinguish the alcoholic, viral, and cholestatic etiologies of diffuse liver disease. ° However, there was no difference between patients with non-alcoholic fatty liver disease (NAFLD) and controls. Sharma et al., using the relative PME intensity as a measure of altered gluconeogenesis (this peak can contain glucose-6-P and 3-phos-phoglycerate in addition to PC and PE), found that hepatic gluconeogenesis was altered in both obese and non-obese Asian Indians with NAFLD, relative to non-obese subjects without NAFLD. 

As mentioned in the introduction, CaMKKs can phosphorylate proteins in addition to CaMKI and CaMKIV. One such alternate target is the AMP-dependent protein kinase (AMPK) (Hawley et al., 1995 Hamilton et al., 2002), and recent studies present compelling evidence that CaMKKs are physiologically relevant activators of AMPK in cultured cells. These studies are of particular interest as AMPK is a kinase intimately involved in the regulation of metabolism, both at the cellular and organismal levels (Kemp et al., 1999). In mammals, AMPK has been implicated in diabetes, obesity and cardiovascular disease (Arad et al., 2002 Kemp et al., 2003) prompting a flurry of studies to identify the relevant AMPKK involved in each tissue that participates in the etiology of these diseases. 

Galgani, J., and Diaz, E. 2000. [Obesity and fatty acids in the etiology of insulin resistance]. Rev MedChil 128 1354-1360. 

It is generally accepted that the primary etiology of obesity concerns problems of energy balance as a consequence of nutritional excess and physical inactivity with less than 1% of cases associated with endocrine dysfunction (13). Changes in body weight or body composition depend on the relationship of energy intake to energy... 

Current predictions suggest that the twin epidemics of obesity and diabetes worldwide will result in an increase in CVD rates, which have sharply declined over the past 30 years, after the introduction of effective lipid-lowering and antihypertensive therapies. The World Health Organization (WHO) reported that in 2002, deaths from CVD outnumbered deaths from the major communicable diseases (AIDS, tuberculosis, and malaria) by 3 to 1 (2). By 2015, an estimated 20 million people will die annually from CVD. Therefore, with the advent of the new millennium, there is a sense of urgency to address the burden of chronic cardiometabolic diseases worldwide. The information on the prevalence and etiology of cardiometabolic diseases, which is cited in this section was obtained from the WHO and Centers for Disease Control (CDC) websites (2-6). 

Even though the mortality from coronary heart disease has declined recently, atherosclerosis and related vascular disorders still are the leading cause of death in the Western world. The etiology of this disease is multifactorial, with hyperlipidemia, smoking, diabetes mellitus, hypertension, and obesity being well-established risk factors for the development of atherosclerosis. Dietary fat affects plasma lipids, lipoproteins, and vascular inflammation and, thus, is linked to atherosclerosis. 

Rimonabant may also alter reward pathways that promote addictive behaviors such as overeating. This drug has been shown to attenuate the rewarding effects of alcohol in a strain of alcohol-preferring rat s (161) and may similarly diminish the pleasurable effects of food and overeating that can often play important roles in the etiology of obesity. 

Introduction - This review will present recent developments on the etiology and treatment of atherosclerosis, hyperlipidemia and cholelithiasis. The other major lipid disorder, obesity, has recently been reviewed as to pathogenesis and treatment,1 new efficacy trials and mechanism of action studies on anorectic agents,2 5 and appetite regulation in normal and abnormal states.3 6... 

This type of UI is known as stress urinary incontinence (SUI). Although the exact etiology of urethral underactivity and SUI in the woman is incompletely understood, clearly identifiable risk factors include pregnancy, childbirth, menopause, cognitive impairment, obesity, and age. The prevalence of SUI in women appears to peak during or after the onset of menopause. This implies that hormonal factors are important in maintaining continence. 

In addition to genetic, behavioral, endocrinal, and other causative factors of obesity, infectious etiology has been known for over two decades... 

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