Obesity is an important risk factor for many serious medical complications, which lead to impaired quality of life, considerable morbidity, premature death, and economic burden. The most common complications of obesity involve alterations in metabolic function that are risk factors for cardiovascular disease (CVD), namely insulin resistance, diabetes, dyslipidemia (increased serum TG and decreased serum HDL-cholesterol), and increased blood pressure. Increased intrahepatic triglyceride content (IHTG; nonalcoholic fatty liver disease) is an important marker of metabolically abnormal obese people. However, not all obese persons develop metabolic complications, and ~25% of obese adults are “metabolically normal” based on insulin sensitivity measured by using the hyperinsulinemic euglycemic clamp technique. In addition, data from the 1994-2004 National Health and Nutrition and Examination Survey (NHANES) found that about one-third of obese adults were metabolically normal, defined as having ≤1 cardiometabolic abnormality (based on blood pressure, homeostasis model assessment of insulin resistance [HOMA-IR] value, and plasma glucose, triglyceride, HDL-cholesterol, and CRP concentrations) and data from the Dallas Heart Study suggest about one-third of obese adults have a normal amount of IHTG. Metabolically-normal obese people are at lower risk of developing future diabetes and CVD than metabolically abnormal obese or metabolically abnormal lean persons, but are usually at higher risk than metabolically normal lean people. The mechanisms responsible for why some obese people are protected from the metabolic complications associated with increased adiposity are not clear but likely involve a series of factors involved in regulating liver, adipose tissue and skeletal muscle biology.