A new study analyzing pairs of identical twins, in which one is obese while the other is a healthy weight, has discovered that "metabolically healthy obesity" in some individuals is linked to lack of adipose tissue inflammation and high mitochondrial function.
Metabolically healthy obesity (MHO) is defined as an individual with a body mass index (BMI) greater than 30, but who does not seem to be at increased risk of the health complications usually associated with excess weight, such as cardiovascular disease and type 2 diabetes.
According to the researchers from the Obesity Research Unit at the University of Helsinki in Finland, the reasons as to why some people maintain MHO has been unclear.
For their study, published in the journal Diabetologia, the research team studied 16 pairs of identical twins aged between 23 and 36-years-old. One of each pair of twins was of a normal weight, while the other was obese.
The researchers examined the body composition of all twins. This included measurements of:
- Abdominal subcutaneous and intra-abdominal fat, and
- Liver fat.
Blood tests and oral glucose tolerance tests were performed on the participants after they had fasted overnight for 12 hours, in order to determine how quickly glucose cleared from the blood.
The participants were measured for lipids present in their blood and certain markers of inflammation, such as apidokines and C-reactive proteins (CRP). The function of the mitochondria and inflammation in the subcutaneous adipose tissue (SAT) was also analyzed.
MHO linked to inflammation and mitochondrial function
In all 16 pairs of twins, the average weight differences between the obese twin and the twin of normal weight was 17 kg.
An identical twin study in which one twin was obese, has linked metabolically healthy obesity to reduced adipose tissue inflammation and high mitochondrial function.
In eight of these pairs, the obese twin showed around a seven times higher amount of liver fat, a 78% increase in insulin production in the oral glucose tolerance test, increased CRP, increased disturbance in their blood fat profile and greater occurrence of high blood pressure.
Furthermore, the obese twins demonstrated various impairments in the mitochondria and chronic inflammation in the SAT - metabolic problems that are likely to lead to disease and complications.
However, in the other eight pairs of identical twins, the obese twin showed no differences from the twin of normal weight in liver fat, insulin sensitivity, CRP, lipids, blood pressure or SAT metabolic characteristics.
From these findings, the study authors note that lack of inflammation in the SAT and high mitochondrial transcription are linked to reduced liver fat and MHO.
The researchers say:
"In our collection of monozygotic twin pairs discordant for obesity, the SAT transcript profile in MHO was characterized by the maintenance of mitochondrial function and absence of inflammation.
Only those individuals that, along with increased obesity, developed SAT dysfunction (low mitochondrial and high inflammatory transcript activity) had fatty livers and the hallmarks of the metabolic syndrome, impaired glucose tolerance and dyslipidaemia."
They continue: "The adipose tissue of the MHO individuals was characterized by the capability for both hypertrophy and hyperplasia of adipocytes with increasing BMI."
The authors note that it is possible MHO may change with age or advanced obesity, but in this study, both metabolically distinct groups were the same age and both showed onset of obesity around the same age.
In conclusion, they note that future studies of MHO characteristics could lead to potential drug targets, particularly in terms of improving mitochondrial function and the prevention of inflammation in adipose tissue.