In a new study published in e-lifeResearchers at the Buck Institute have uncovered why some chemicals found in prepared or processed foods can lead to increased hunger and a decreased ability to make healthy food choices. These chemicals, known as advanced glycation end products, are associated with overeating and obesity. This research is particularly important because it provides insight into factors contributing to the global obesity epidemic and may help inform strategies for healthier eating habits.
Advanced glycation end products, often referred to as AGEs, are a group of complex compounds formed when sugars (carbohydrates) chemically react with proteins, lipids (fats), or nucleic acids (such as DNA) in a process known as glycation. is. This reaction usually occurs slowly in our bodies as a natural part of aging and metabolism.
But AGEs can also form more rapidly when foods are cooked or processed at high temperatures, such as grilling, frying, or baking. This more advanced stage of saccharification is known as the Maillard reaction and is responsible for browning and developing desirable flavors in cooked and processed foods.
AGEs are responsible for the appealing color, taste, and aroma of cooked or processed foods. Think crispy crust on bread, browned steak, and golden brown on baked goods. All of this is partly due to the formation of AGEs.
“This research, conducted using tiny worms, has enormous implications for human dietary choices and our tendency to overeat certain foods,” said the study’s senior author. jubify health. “Modern processed foods rich in AGEs are tempting to eat, but little is known about their long-term effects on our health.”
“Humans have evolved certain mechanisms that encourage us to eat as much food as possible when food is plentiful. We store excess calories as fat and use them to survive periods of fasting.” Postdoctoral researcher Muneeshu Mutayan Shanmugam explained. Kapahi Laboratory, and lead author of the study. “Natural selection has favored genes that preferentially consume flavorful foods, especially those high in sugar. But what are the mechanisms that make it difficult to say ‘no’ to them?”
To investigate the effects of AGEs on feeding behavior and a potential link to obesity, researchers conducted experiments using C. elegans. Caenorhabditis elegans, as a model organism. Despite their simplicity, these tiny insects share important biological pathways with humans, making them valuable research tools.
The study involved analyzing the behavior of C. elegans when exposed to AGEs, specifically one type of AGE called MG-H1. The researchers found that both genetically engineered worms lacking systems to detoxify AGEs and worms exposed to MG-H1 showed increased feeding behavior. This suggests that AGE accumulation due to genetic factors or dietary intake may lead to overeating.
“I was surprised by the fact that AGEs are enough to increase food consumption. This explains why we cook our food so much,” Kapahi told Cypost.
Additionally, worms lacking the glyoxalase system that detoxifies compounds like MG-H1 had significantly shorter lifespans. This highlights the potential long-term health effects of AGEs, even in organisms as small as C. elegans.
Researchers dug deeper to understand the mechanisms behind this increase in eating behavior. They identified a specific signaling pathway involving the elt-3 GATA transcription factor that controls the expression of the tdc-1 gene (tyramine decarboxylase) and tyramine receptors (tyra-2 and ser-2). This pathway is responsible for mediating the negative effects of AGEs, such as increased food intake, shortened lifespan, and neurological damage.
Importantly, this study is the first to identify this specific signaling pathway mediated by the AGE MG-H1 and its effects on feeding and neurodegeneration. These findings highlight the detrimental effects of AGEs and their contribution to diseases such as obesity and neurodegeneration.
“Understanding this signaling pathway may help us understand overeating due to modern AGE-rich diets,” Kapahi said. “Our research highlights that the accumulation of AGEs is involved in diseases such as obesity and neurodegeneration. We believe this is related to the global increase in age-related diseases.”
This research helps us understand why certain foods are difficult to resist, leading to overeating and weight gain. It also highlights that AGEs in the diet have a negative impact not only on body weight but also on health, including the brain.
The study results show that “sugar glycation is the main cause of sugar’s negative effects,” Kapahi told SciPost. “It also means you should boil and stalk your food instead of cooking it over a dry fire, which produces AGEs. Every time you toast, you produce more than 50 new AGEs.”
Although this study provides valuable insight into how AGEs affect feeding behavior and health, C. elegans is a simple organism and discoveries in these nematodes have direct implications for humans. It is important to note that this may not always be the case.
“We need to measure more carefully whether this also applies to humans,” Kapahi said. “However, some studies indirectly support this, as reducing foods containing AGEs is good for your health.”
Limiting the accumulation of AGEs may have important relevance for improving public health, as AGEs are associated with various age-related diseases such as obesity and neurodegeneration. The findings suggest that careful dietary choices, including cooking methods and food choices, can reduce the impact of AGEs on our health and well-being.
“My lab also produced a supplement called GLYLO that reduces the formation of AGEs. We found that this supplement helped slow aging and improve glucose metabolism in mice.”
the study, “Methylglyoxal-derived hydroimidazolone MG-H1 increases food intake by altering tyramine signaling through the C. elegans GATA transcription factor ELT-3” by Muneeshu Muthayan Shanmugam, Jyotiska Chaudhuri, Durai Selegunder, Amit Kumar Sahu, Sanjiv Guha, Manish Chamoli, Brian Hodge, Neelanjan Bose, Caris Roberts, Dominic O. Farella, Published by Gordon Lithgow, Richmond Sarpong, James J. Galligan, Pankaj Kapahi. .
