In a recent study published in Scientific Reports, researchers investigated the association of different types of obesity with serum leptin (LEP) and adiponectin (ADP) levels.
The global obesity epidemic has led to a dramatic surge in metabolic diseases in the last 10 years. Interestingly, not all obese people develop metabolic syndrome (MS), a common complication of obesity that leads to chronic diseases such as hypertension and diabetes.
There are well-defined diagnostic criteria for MS, which take into account an individual's biological sex, waist circumference (WC), serum triglyceride (TG), fasting insulin (FINS), fasting plasma glucose (FPG) levels, and blood pressure (BP).
Moreover, there are well-established parameters for body mass index (BMI) and weight for all adults.
The absence of MS characterizes people with metabolically healthy obesity (MHO), while other obese people fall in the category of metabolically unhealthy obesity (MUO).
Previous studies have indicated that individuals with MHO do not have metabolic abnormalities and lower inflammation levels than those with MUO.
Moreover, these studies indicated that healthy people and those with MHO have lower WC, BMI, TG, homeostasis model assessment of insulin resistance (Homa-IR), FINS, BP, and high-density lipoprotein-cholesterol (HDL-C).
Furthermore, people with MHO have lower LEP but higher ADP levels than those with MUO. However, their expression levels across obesity phenotypes compared to healthy individuals remain unclear.
LEP and ADP are adipokines secreted by the adipose tissue, a crucial endocrine organ. Any disruption to adipokine secretion due to loss of inflammatory balance could lead to metabolic diseases, especially type 2 diabetes (T2D) and cardiovascular diseases (CVDs).
A study by Hotamisligil et al. demonstrated a strong correlation between metabolic dysfunction and immune response, manifesting as a cluster of chronic metabolic disorders. These diseases maintain the body in a state of chronic low-grade inflammation.
LEP plays a crucial role in the energy homeostasis of all cell types in the body by promoting glucose utilization and improving insulin sensitivity. Moreover, it displays a positive correlation with body fat mass.
On the other hand, ADP, an anti-inflammatory hormone, via its physiological functions, such as insulin sensitization, glucose metabolism, and lipid oxidation, prevents obesity-related cardiometabolic issues. Accordingly, both LEP and ADP are considered markers for MS.
About the study
In the present study, researchers analyzed data from 178 participants of a cross-sectional survey conducted in Xinjiang, China, to form three cohorts.
The MUO and MHO groups comprised 99 and 31 subjects, respectively, with a BMI ≥ 24 kg/m2. While the individuals in the former group met the diagnostic criteria of MS (two or more), those in the MHO group met none or only one MS diagnostic criterion (excluding WC).
All 48 individuals in the healthy control (HC) group had average body weight, with BMI ≥18.5 kg/m2 but less than 24 kg/m2. The researchers excluded participants who were pregnant, lactating, or suffering from cancer, hepatic, renal, and cardiovascular diseases.
The team collected fasting blood samples from each subject to determine serum TG levels and total cholesterol (TC), including HDL-C and LDL-C, FPG, and FINS. They used this data to calculate Homa-IR. Further, they quantified serum ADP and LEP levels using commercially available enzyme-linked immunosorbent assay (ELISA) kits.
The team used a t-test and rank sum test to compare all study groups, presenting data as percentiles or standard deviation (SD). Additionally, they performed Pearson correlation analysis to draw a correlation between obesity phenotypes and LEP and ADP levels, where a p-value <0.05 was considered statistically significant.
Of 178 study subjects, 105 were females, 73 were males, and their average age and BMI were 41.89±11.42 years and 27.33 ± 4.58 kg/m2, respectively.
Elevated FINS and Homa-IR in MHO and MUO groups indicated these individuals had hyperinsulinemia. However, since the MUO group had markedly elevated serum levels of FPG, they were more prone to developing T2D than individuals with MHO.
Moreover, BP levels across the two study groups were different. Furthermore, the results indicated a correlation between increased BMI and hypertension risk.
As an MS marker, ADP exhibited an inverse correlation with WC, visceral fat, BP, blood lipids, and plasma glucose and insulin levels. On the other hand, it showed a negative correlation with FPG in the MHO group.
Likewise, the authors noted a positive correlation of LEP with WC, waist-hip ratio (WHR), BMI, and fat mass. The observed elevation in plasma levels of LEP in the MHO group showed a positive correlation with FINS and Homa-IR in the MUO group. Interestingly, the correlation of BMI with LEP was independent across both obesity phenotypes.
Of all the parameters assessed, BP, WC, BMI, WHR, TG, TC, LDL-C, FINS, FPG, and Homa-IR were markedly higher in the MUO versus MHO group.
The correlation analysis also suggested that people with MUO were more susceptible to developing glucose and lipid metabolism-related disorders than people with MHO.
Even though ADP and LEP levels across individuals with MHO and MUO were not markedly different, both adipokines showed a clear correlation with glucose utilization and lipid metabolism-related parameters in both obesity phenotypes.
Since alterations in ADP and LEP levels might manifest as obesity-related metabolic disorders, future research should explore their association with obesity phenotypes further.