A popular yet often ineffective way to lose body weight is Dieting as the majority of people regain most of their pre-dieting weights in a comparatively short time. However, the underlying molecular mechanisms of weight regain and the increased risk for the metabolic disease remains unclear. 

A study investigated the molecular alterations inherited from a history of obesity. They considered male high-fat diet (HFD)-fed obese C57BL/6J mice that were altered to a low caloric chow diet, causing a drop in body weight similar to lean mice. 

Body composition, metrics of glucose, insulin and lipid homeostasis were measured along with histological and gene expression analysis of adipose tissue and liver to evaluate adipose tissue inflammation and hepatosteatosis. Further, qPCR was utilized to evaluate acute hypothalamic response to (re-) exposure to HFD.

 The observations were as follows-

• Most obesity-associated phenotypes like body mass, glucose intolerance and blood metabolite levels reversed Within 7 weeks of diet switch. 
• Yet, hepatic inflammation, hepatic steatosis, hypertrophy and inflammation of perigonadal, except subcutaneous, adipocytes continued in previously obese mice. 
• Transcriptional profiling of liver and perigonadal fat showed an upregulation of pathways related to immune function and cellularity. 

Thus it was proved that weight reduction still leaves some amount of inflammation in the liver and perigonadal fat, which could increase the risk of formerly obese subjects for developing the metabolic syndrome upon recurring weight gain.

Source- Int J Obes,2018;42: 507–517. https://doi.org/10.1038/ijo.2017.224