What follows summarizes the major issues addressed and the outcomes of the discussion. However, the precise mechanisms linking the two conditions remain unclear, as does our understanding of interindividual differences.
Obesity-associated cellular injury can in turn recruit and activate macrophages and other immune cells that exacerbate tissue inflammation 23 Increased upper body fat including visceral adiposity, as reflected in increased abdominal girth or waist-to-hip ratio, is associated with the metabolic syndrome, type 2 diabetes, and cardiovascular disease 3although underlying mechanisms remain uncertain.
Obesity-induced glucose intolerance reflects failure to mount one or more of these compensatory responses These intriguing, but still largely unexplored, connections between obesity and type 2 diabetes suggested the timely need to convene a group of scientific experts in the fields to more closely examine underlying pathophysiology and treatment options for patients with type 2 diabetes addressing issues of excess weight and glycemic control simultaneously.
Managing body weight by behavioral change and medications The dramatic increase in incidence and prevalence of obesity over the past 50 years, associated in part with major worldwide changes in caloric intake and dietary composition, has focused attention on lifestyle intervention to reverse or ameliorate caloric imbalance.
Table 1 lists medications that have been available and others under development. Not surprisingly, many obesity gene variants appear to be involved in pathways affecting energy homeostasis. Beyond differences in body fat distribution, emerging evidence suggests that different subtypes of adipose tissue may be functionally distinct and affect glucose homeostasis differentially.
Likewise, adipose tissue is composed of heterogeneous cell types. Participants reviewed and discussed published literature and their own unpublished data. Collectively, these responses contribute to the pathogenesis of insulin resistance in the liver, skeletal muscle, and adipose tissue, and some e.
One potential link could be sustained cell Research paper on obesity and diabetes to nutrient concentrations exceeding energy requirements.
Mechanisms of obesity-associated insulin resistance The influence of obesity on type 2 diabetes risk is determined not only by the degree of obesity but also by where fat accumulates. Although additional genes with important roles will undoubtedly be discovered, this low predictive power may reflect the importance of environmental factors, less frequent genetic variants with stronger effects, or gene-environment, gene-gene, and epigenetic interactions that are not readily identified through methods based on population genetics.
For example, recent rodent studies have demonstrated diabetogenic effects of reduced pancreatic expression of the Pdx1 gene 14 Improved understanding will help advance identification and development of effective treatment options. Improved understanding of how obesity relates to type 2 diabetes may help advance effective and cost-effective interventions for both conditions, including more tailored therapy.
Immune cells within adipose tissue also likely contribute to systemic metabolic processes. To expedite this process, we recommend further investigation into the pathogenesis of these coexistent conditions and innovative approaches to their pharmacological and surgical management.
Adult humans have limited and variable numbers of brown fat cells 4which play a role in thermogenesis and potentially influence energy expenditure and obesity susceptibility 5. One should also keep in mind that the missing heritability could be an illusion of inferring additive genetic effects from epidemiological data If obesity is associated with impairment of neurocircuits regulating both energy balance and insulin action, obesity-induced insulin resistance may arise not only as a direct consequence of excessive adipose mass but via neuronal mechanisms as well.
Further genetic studies may elucidate additional common pathophysiological pathways for obesity and diabetes and identify promising new treatment targets. Medications have been used to assist in weight loss for almost 80 years, but adverse effects frequently restrict utility.
Alternatively, pathway analyses or a systems biology approach combining information from DNA variations with transcript, protein, and metabolite profiles may better capture the genetic influences on metabolism than studying single genes.
At least three distinct mechanisms have been proposed to link obesity to insulin resistance and predispose to type 2 diabetes: Methods for detecting gene-gene interactions exist, but the population size needed to detect them is substantially greater than is required for detection of single genes of relatively small effect.
For example, short-term intervention studies suggest that dietary changes, which emphasize less fat and refined carbohydrates, make it easier to reduce total caloric intake in obese adults and overweight children 30 Successful lifestyle intervention programs typically involve self-monitoring of weight, dietary intake, and activity; behavioral modification; frequent contact; and caloric balance through diet, with or without exercise.
Brain neurocircuits governing energy homeostasis also affect insulin sensitivity in the liver and perhaps other peripheral tissues 25and inflammation similar to that induced by obesity in peripheral insulin-sensitive tissues also occurs in these areas of the brain As the study of adipose biology progresses, it will be important to consider whether additional subtypes of adipocytes or other cell types can be identified to refine our understanding of obesity complications and generate novel approaches to prevention.
These interactions are complex, with the relative importance of each unclearly defined.
Although mechanisms underlying this coupling e. A writing group comprising eight participants subsequently prepared this summary and recommendations. Furthermore, concern regarding adverse effects, including cardiovascular disease risk and central effects e. Excess weight is an established risk factor for type 2 diabetes, yet most obese individuals do not develop type 2 diabetes.
Reduced insulin secretion can in turn worsen the nutrient excess problem by raising circulating concentrations of glucose, free fatty acids, and other nutrients.A research paper on obesity and diabetes discuss how obesity can cause insulin resistance that prevents the body from self-regulating insulin levels.
OBJECTIVE This report examines what is known about the relationship between obesity and type 2 diabetes and how future research in these areas might be directed to benefit prevention, interventions, and overall patient care.
RESEARCH DESIGN AND METHODS An international working group of 32 experts in the pathophysiology, genetics, clinical trials, and clinical care of obesity and/or type 2.
Obesity is a major risk factor for Type 2 diabetes. At Cedars-Sinai, we have recognized the close linkage between diabetes and obesity by establishing the world class Cedars-Sinai Diabetes and Obesity Research Institute in Los Angeles.
This paper will look at the analysis of diabetes in young children, obesity, health education strategies and communication strategies used in nursing care and control of diabetes (Benjamin,). 16 Hot Topics in Diabetes Research Today. We've tapped some of the top researchers, clinicians, and advisers in diabetes care -- including our editorial advisory board members -- to focus on the most current and useful findings.
At the Forefront of Diabetes Research Experts point to rising obesity rates as a main culprit of type 2. Free Obesity papers, essays, and research papers Obesity affects both adults and children but it is more chronic to young children. This paper will look at the analysis of diabetes in young children, obesity, health education strategies and communication strategies used in nursing care and control of diabetes (Benjamin,Download