Metabolic and body composition factors in subgroups of obesity: what do we know?

Obesity is thought to be a heterogeneous disorder with several possible etiologies; therefore, by examining subtypes of obesity we attempt to understand obesity's heterogeneous nature. The purpose of this review was to investigate the roles of metabolic, body composition, and cardiovascular disease risk in subtypes of obesity. We briefly consider two subtypes of obesity that have been identified in the literature. One subset of individuals, termed the metabolically healthy, but obese (MHO), despite having large amounts of fat mass compared with at risk obese individuals shows a normal metabolic profile, but remarkably normal to high levels of insulin sensitivity. Preliminary evidence suggests that this could be due at least in part to lower visceral fat levels and earlier onset of obesity. A second subset, termed the metabolically obese, but normal weight (MONW), present with normal body mass index, but have significant risk factors for diabetes, metabolic syndrome, and cardiovascular disease, which could be due to higher fat mass and plasma triglycerides as well as higher visceral fat and liver content. We also briefly consider the potential role of adipose and gastrointestinal hormonal profiles in MHO and MONW individuals, which could lead to a better understanding of potential factors that may regulate their body composition. This information will eventually be invaluable in helping us understand factors that predispose to or protect obese individuals from metabolic and cardiovascular disease. Collectively, a greater understanding of the MHO and MONW individual has important implications for therapeutic decision making, the characterization of subjects in research protocols, and medical education.

[1]  E. Gabazza,et al.  Increased visceral fat and serum levels of triglyceride are associated with insulin resistance in Japanese metabolically obese, normal weight subjects with normal glucose tolerance. , 2003, Diabetes care.

[2]  Y. Matsuzawa,et al.  Pathophysiology and molecular mechanisms of visceral fat syndrome: the Japanese experience. , 1997, Diabetes/metabolism reviews.

[3]  J. Després,et al.  Low‐intensity endurance exercise training, plasma lipoproteins and the risk of coronary heart disease , 1994, Journal of internal medicine.

[4]  E. Ferrannini,et al.  Insulin resistance and hypersecretion in obesity. European Group for the Study of Insulin Resistance (EGIR). , 1997, The Journal of clinical investigation.

[5]  A. Häkkinen,et al.  Fat accumulation in the liver is associated with defects in insulin suppression of glucose production and serum free fatty acids independent of obesity in normal men. , 2002, The Journal of clinical endocrinology and metabolism.

[6]  E. Bleecker,et al.  Effects of weight loss vs aerobic exercise training on risk factors for coronary disease in healthy, obese, middle-aged and older men. A randomized controlled trial. , 1995, JAMA.

[7]  L. Sjöström,et al.  The morphology and metabolism of intraabdominal adipose tissue in men. , 1992, Metabolism: clinical and experimental.

[8]  N. Ruderman,et al.  Obesity-associated disorders in normal-weight individuals: some speculations. , 1982, International journal of obesity.

[9]  K. Frayn,et al.  Adipose tissue as a buffer for daily lipid flux , 2002, Diabetologia.

[10]  M. Laakso,et al.  Insulin Action and Age: European Group for the Study of Insulin Resistance (EGIR) , 1996, Diabetes.

[11]  E. Ferrannini,et al.  Influence of duration of obesity on the insulin resistance of obese non-diabetic patients , 1998, International Journal of Obesity.

[12]  S. Cushman,et al.  Studies of human adipose tissue. Adipose cell size and number in nonobese and obese patients. , 1973, The Journal of clinical investigation.

[13]  P. Havel Control of energy homeostasis and insulin action by adipocyte hormones: leptin, acylation stimulating protein, and adiponectin , 2002, Current opinion in lipidology.

[14]  S. Haffner,et al.  Hyperinsulinaemia: the key feature of a cardiovascular and metabolic syndrome , 1991, Diabetologia.

[15]  C. Mantzoros,et al.  Hypoadiponectinemia is associated with insulin resistance, hypertriglyceridemia, and fat redistribution in human immunodeficiency virus-infected patients treated with highly active antiretroviral therapy. , 2003, The Journal of clinical endocrinology and metabolism.

[16]  H. K. Lee,et al.  Intra-abdominal fat is associated with decreased insulin sensitivity in healthy young men. , 1991, Metabolism: clinical and experimental.

[17]  E. A. Sims,et al.  What are the physical characteristics associated with a normal metabolic profile despite a high level of obesity in postmenopausal women? , 2001, The Journal of clinical endocrinology and metabolism.

[18]  E. Bonora,et al.  Risk factors for coronary artery disease in healthy persons with hyperinsulinemia and normal glucose tolerance. , 1989, The New England journal of medicine.

[19]  G. Dimcevski,et al.  Intra-abdominal obesity and metabolic risk factors: a study of young adults* , 2003, International Journal of Obesity.

[20]  E. Gabazza,et al.  Plasma levels of adiponectin are associated with insulin resistance and serum levels of triglyceride in Japanese metabolically obese, normal-weight men with normal glucose tolerance. , 2003, Diabetes care.

[21]  K. Kangawa,et al.  Fasting plasma ghrelin levels are negatively correlated with insulin resistance and PAI-1, but not with leptin, in obese children and adolescents. , 2002, Diabetes.

[22]  E. Poehlman,et al.  Dvorak RV, DeNino WF, Ades PA, Poehlman ET. Phenotypic characteristics associated with insulin resistance in metabolically obese but normal-weight young women. Diabetes 48: 2210-2214 , 1999 .

[23]  A. Astrup,et al.  Obesity : Preventing and managing the global epidemic , 2000 .

[24]  R. Andres Effect of obesity on total mortality. , 1980, International journal of obesity.

[25]  P. Froguel,et al.  A variation in the ghrelin gene increases weight and decreases insulin secretion in tall, obese children. , 2002, The Journal of clinical endocrinology and metabolism.

[26]  E. A. Sims,et al.  Are there persons who are obese, but metabolically healthy? , 2001, Metabolism: clinical and experimental.

[27]  R. Vettor,et al.  Resistin and adiponectin expression in visceral fat of obese rats: effect of weight loss. , 2002, Obesity research.

[28]  H. Vidal,et al.  Differences in mRNA expression of the proteins secreted by the adipocytes in human subcutaneous and visceral adipose tissues. , 2000, Biochimica et biophysica acta.

[29]  H. Oflaz,et al.  Determination of endothelial function and early atherosclerotic changes in healthy obese women. , 2003, Diabetes, nutrition & metabolism.

[30]  S. Kiechl,et al.  Prevalence of insulin resistance in metabolic disorders: the Bruneck Study. , 1998, Diabetes.

[31]  N. Ruderman,et al.  The "metabolically-obese," normal-weight individual. , 1981, The American journal of clinical nutrition.

[32]  E. Poehlman,et al.  Obesity, body fat distribution, and coronary artery disease. , 2000, Journal of cardiopulmonary rehabilitation.

[33]  E. Ravussin,et al.  Circulating ghrelin levels are decreased in human obesity. , 2001, Diabetes.

[34]  Am Sharma Adipose tissue: a mediator of cardiovascular risk , 2002, International Journal of Obesity.

[35]  E. Poehlman,et al.  Phenotypic characteristics associated with insulin resistance in metabolically obese but normal-weight young women. , 1999, Diabetes.

[36]  H. Koistinen,et al.  Plasma Acylation Stimulating Protein Concentration and Subcutaneous Adipose Tissue C3 mRNA Expression in Nondiabetic and Type 2 Diabetic Men , 2001, Arteriosclerosis, thrombosis, and vascular biology.

[37]  D. Chisholm,et al.  The metabolically obese, normal-weight individual revisited. , 1998, Diabetes.

[38]  D. Matthews,et al.  Systemic resistance to the antilipolytic effect of insulin in black and white women with visceral obesity. , 1999, American journal of physiology. Endocrinology and metabolism.