Welcome to The Weekly Gene, a blog series brought to you by Helix that introduces a different human gene each week. We’ll share important facts, relevant research, and how these genes might be related to certain conditions and traits. It’s a great way to build your DNA vocabulary, learn more about the code that makes all of us unique, and find a path to the genetic insights that are important to you.
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Take a deep breath before saying this one: Peroxisome Proliferator-Activated Receptor Gamma. (Fortunately, you can just call it PPARG, pronounced “pee-par-gamma.”) This protein plays a role in determining body weight through its involvement in the metabolism of fats and sugars. PPARG controls the body’s ability to retain fat by translating DNA that codes for proteins involved in fat development. Interestingly, new findings suggest that small variations in an individual’s PPARG gene may influence how quickly their body gains or loses weight under specific conditions.
Your DNA contains instructions for how to make proteins, functional parts of a cell that carry out specific tasks (structural support, cellular defense, cell-to-cell communication, and so on). Occasionally, changes will occur in the DNA sequence—so-called variations—which can change the proteins that are produced. A good example is the PPARG gene, where there are known variations that cause the protein to lose functionality and ultimately affect the body’s regulation of fat and sugar metabolism.
Knowing your genetics could help you design a diet plan that works better for you
To make proteins from DNA, a cell undergoes a process known as transcription. During this process, information coded within the DNA sequence is copied into a short-lived string of bases known as RNA. PPARG is a special kind of protein known as a transcription factor, a class of proteins that helps transcribe DNA sequences into RNA. Like DNA, RNA contains information for creating proteins (among other functions). This is an important process because DNA is largely restricted to a cell’s nucleus, so instructions within the DNA need to be exported out of the nucleus to where proteins are built. To do this, transcription factors bind to the DNA and initiate the transcription process.
PPARG is one of these proteins and is able to initiate the transcription of genes associated with fat tissue development. Multiple variations have been identified in DNA which result in loss of the protein’s function, with the most common being a single base change that decreases the protein’s ability to bind with DNA. When this happens, its ability to transcribe DNA (and subsequently, the production of proteins) is impaired.
PPARG may have an impact on BMI and weight, research suggests
Since its discovery in 1997, this PPARG variant has been the subject of intense research focusing on its potential role in body mass index (BMI). These efforts have revealed that decreased functionality of the PPARG gene may result in a complex change in how the body responds to high-fat diets, potentially influencing the body’s tendency to gain or lose weight. In some instances, researchers have found that loss of functionality from the PPARG gene results in less weight gain when compared to control participants on a high fat diet1. At the same time, these authors also found the PPARG gene variant to be associated with less weight loss after a specific diet routine.
This preliminary study indicates a complex interplay between PPARG and BMI, and sheds some light on how the unique combination of our genetic predispositions and diet can affect us. Knowing which PPARG variant you have could help you design a diet plan that works better for you. Products on the Helix marketplace like Fitness Diet Pro and embodyDNA combine genetic insights—including genes like PPARG—with personalized diet and workout recommendations to help you pursue a healthy lifestyle.
1Garaulet, Marta et al. “PPARγ Pro12Ala Interacts with Fat Intake for Obesity and Weight Loss in a Behavioural Treatment Based on the Mediterranean Diet.” Molecular nutrition & food research 55.12 (2011): 1771–1779. PMC. Web. 12 Sept. 2017.