Obesity increases risk for chronic diseases. Metabolically unhealthy obese (MUO) individuals exhibit obesity-related metabolic abnormalities, while metabolically healthy obese (MHO) individuals do not. Controversy exists over whether MHO is a transient state prior to metabolic disease development, which is significant as estimates suggest 5-30% of obese individuals are MHO. Like humans, nonhuman primates (NHP) demonstrate these same classifications despite optimal dietary environments.
Here, we replicated and validated findings where we had characterized MHO and MUO obesity subtypes in a NHP model using metabolic syndrome criteria (increased waist circumference [>40cm], blood pressure, glycemic dysregulation [elevated glycosylation of hemoglobin or fasting glucose], and decreased high density lipopoprotein cholesterol). MHO subjects were classified as those with no risk factors while MUO subjects were classified as those with a ≥1 additional risk factors.
Of 112 adult vervet monkeys, 23% were obese. There were no differences in sex distribution, age, or weight/waist circumference across obese subjects; we found that 38% were MUO and 42% were MHO. By design, risk scores for the MUO were significantly higher. These prevalences align with human data. MUO subjects exhibited significantly increased fasting blood glucose, triglycerides (both p<0.01) and a trend toward increased percent glycosylation of hemoglobin (p=0.09). No blood pressure or HDL-c differences were observed.
We successfully repeated our characterization of MHO and MUO obesity subtypes in a nonhuman primate model, which is a phenotype not faithfully replicated in any other animal model. Next, we will investigate the transgenerational nature of obesity subtypes by assessing the growth patterns of MHO/MUS offspring.