You can find capsules of gamma-aminobutyric acid [GABA] in almost every supplements shop. GABA promotes sleep and is a growth hormone enhancer, but GABA supplements can also help obese people to stay healthy. According to researchers at the University of California Los Angeles, GABA inhibits the increase in fat reserves that otherwise happens if you eat more calories than you burn. This is because GABA makes your cells more sensitive to insulin.
The more body fat you have, the less sensitive your cells are to insulin. This is primarily because large fat deposits are subject to inflammation, as a result of which they secrete substances that sabotage the functioning of insulin. The researchers already published an animal study in 2004 in which they had shown that GABA [structural formula shown above] inhibits this process.
The man said he had been preparing for a competition and had started a cycle of anabolic steroids six weeks before. He had been taking 100 mg methandrostenolone daily. The bodybuilder used Body Research’s Danabol, which he had bought from a Thai web store.
In another animal study, published in PLoS One in 2011, the researchers fattened mice for 20 weeks by putting them on a high fat diet [HFD]. Half of the animals were also given GABA in their drinking water.
The human equivalent of the dose they used was 800-1200 mg GABA daily.
Supplementation with GABA did not reduce food intake, but did reduce weight increase. In the body the GABA supplementation inhibited the growth of fat reserves.
When the researchers gave their lab animals glucose and insulin, the glucose disappeared more quickly from the blood of the mice that had been given GABA. This implies that GABA boosted the mice’s sensitivity to insulin.
The fat tissue of the GABA mice contained fewer immune cells than that of the mice in the other group. That means that the inflammations in the fat tissue were less strong. GABA probably works via the immune system.
At the end of the 20 weeks the researchers gave their mice a standard diet again, but continued the supplementation. The body weight and glucose level stabilised in the GABA group, but deteriorated in the other group.
“Given that GABA mainly acts on the peripheral GABA receptors and is safe for human consumption, GABA and other GABAA-R agonists may be valuable for the prevention and treatment of obesity and type-2 diabetes mellitus in the clinic”, the researchers conclude.
Jide Tian, the first author of the study and Daniel Kaufman, head of the research are convinced. So convinced that they have patented the method they discovered. [EP 2621282 A2.]
Oral treatment with ?-aminobutyric acid improves glucose tolerance and insulin sensitivity by inhibiting inflammation in high fat diet-fed mice.
Adipocyte and ?-cell dysfunction and macrophage-related chronic inflammation are critical for the development of obesity-related insulin resistance and type 2 diabetes mellitus (T2DM), which can be negatively regulated by Tregs. Our previous studies and those of others have shown that activation of ?-aminobutyric acid (GABA) receptors inhibits inflammation in mice. However, whether GABA could modulate high fat diet (HFD)-induced obesity, glucose intolerance and insulin resistance has not been explored. Here, we show that although oral treatment with GABA does not affect water and food consumption it inhibits the HFD-induced gain in body weights in C57BL/6 mice. Furthermore, oral treatment with GABA significantly reduced the concentrations of fasting blood glucose, and improved glucose tolerance and insulin sensitivity in the HFD-fed mice. More importantly, after the onset of obesity and T2DM, oral treatment with GABA inhibited the continual HFD-induced gain in body weights, reduced the concentrations of fasting blood glucose and improved glucose tolerance and insulin sensitivity in mice. In addition, oral treatment with GABA reduced the epididymal fat mass, adipocyte size, and the frequency of macrophage infiltrates in the adipose tissues of HFD-fed mice. Notably, oral treatment with GABA significantly increased the frequency of CD4(+)Foxp3(+) Tregs in mice. Collectively, our data indicated that activation of peripheral GABA receptors inhibited the HFD-induced glucose intolerance, insulin resistance, and obesity by inhibiting obesity-related inflammation and up-regulating Treg responses in vivo. Given that GABA is safe for human consumption, activators of GABA receptors may be valuable for the prevention of obesity and intervention of T2DM in the clinic.
PMID: 21966503 PMCID: PMC3178643 DOI: 10.1371/journal.pone.0025338 [PubMed – indexed for MEDLINE] Free PMC Article