Scientists in China have identified a gene that could enhance resistance to obesity, potentially unraveling the complex mechanisms behind this global health issue.

Obesity is associated with numerous serious health conditions, including cardiovascular diseases and type 2 diabetes.

As medical research progresses, humanity's understanding&nbsp;of obesity and its health implications continues to grow.

While diet and lifestyle factors are crucial, a recent study led by Professor Jin Li and Associate Professor Zheng Hongxiang from Fudan University points to the&nbsp;role of genetics in determining the intensity of obesity.

The team analysed 2,877 samples from three independent populations in Guangxi, Jiangsu, and Henan.

Their findings were published in the peer-reviewed Journal of Genetics and Genomics.

<h2>Genetics and Obesity: What is the link?</h2>

The study identified a type of mitochondrial DNA prevalent in southern China and Southeast Asia that appears to protect against obesity.

"Mitochondria are often referred to as the cell’s powerhouses, generating 80 to 90 percent of the energy needed for various human behaviors. Mitochondrial function has long been associated with obesity," Jin wrote.

Also read |&nbsp;<a href="https://www.wionews.com/science/does-obesity-really-increase-risk-of-dementia-or-is-it-the-opposite-718061">Does obesity really increase risk of dementia or is it the opposite?</a>

Unlike nuclear DNA, inherited from both parents, mitochondrial DNA is passed down only from the mother and is more prone to genetic mutations.

Jin and his colleagues performed association analyses of 16 basal mitochondrial DNA haplogroups, genetic families tracing back to a common ancestor.

They discovered that a specific variant group, M7, consistently correlated with a reduced risk of obesity.

Further analysis pinpointed the M7b1a1 subgroup as its most likely source.

Also watch |&nbsp;Obesity fuelling 32 types of cancer: Research

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A 2019 study by Professor Kong Qingpeng from the Chinese Academy of Sciences, published in Molecular Biology and Evolution, revealed that M7b1a1 is primarily found in southern China and mainland Southeast Asia, with significant frequencies among southern Han Chinese individuals, ranging from 5 to 14 per cent.

Jin suggested that reduced mitochondrial function might explain why M7b1a1 lowers obesity risk.

"Decreased mitochondrial functions represent less energy conservation and more heat production, which could result in less weight gain," he wrote.

"Our findings offer new insights into the genetic basis of obesity-related traits, enhancing our understanding of how genetics can influence body fat distribution and obesity risk," Jin concluded.

Scientists in China have identified a gene that could enhance resistance to obesity, potentially unraveling the complex mechanisms behind this global health issue.

Scientists in China have identified a gene that could enhance resistance to obesity, potentially unraveling the complex mechanisms behind this global health issue. Obesity is associated with numerous serious health conditions, including cardiovascular diseases and type 2 diabetes. As medical research progresses, humanity's understanding of obesity and its health implications continues to grow. While diet and lifestyle factors are crucial, a recent study led by Professor Jin Li and Associate Professor Zheng Hongxiang from Fudan University points to the role of genetics in determining the intensity of obesity. The team analysed 2,877 samples from three independent populations in Guangxi, Jiangsu, and Henan. Their findings were published in the peer-reviewed Journal of Genetics and Genomics. Genetics and Obesity: What is the link? The study identified a type of mitochondrial DNA prevalent in southern China and Southeast Asia that appears to protect against obesity. "Mitochondria are often referred to as the cell’s powerhouses, generating 80 to 90 percent of the energy needed for various human behaviors. Mitochondrial function has long been associated with obesity," Jin wrote. Also read | Does obesity really increase risk of dementia or is it the opposite? Unlike nuclear DNA, inherited from both parents, mitochondrial DNA is passed down only from the mother and is more prone to genetic mutations. Jin and his colleagues performed association analyses of 16 basal mitochondrial DNA haplogroups, genetic families tracing back to a common ancestor. They discovered that a specific variant group, M7, consistently correlated with a reduced risk of obesity. Further analysis pinpointed the M7b1a1 subgroup as its most likely source. Also watch | Obesity fuelling 32 types of cancer: Research × A 2019 study by Professor Kong Qingpeng from the Chinese Academy of Sciences, published in Molecular Biology and Evolution, revealed that M7b1a1 is primarily found in southern China and mainland Southeast Asia, with significant frequencies among southern Han Chinese individuals, ranging from 5 to 14 per cent. Jin suggested that reduced mitochondrial function might explain why M7b1a1 lowers obesity risk. "Decreased mitochondrial functions represent less energy conservation and more heat production, which could result in less weight gain," he wrote. "Our findings offer new insights into the genetic basis of obesity-related traits, enhancing our understanding of how genetics can influence body fat distribution and obesity risk," Jin concluded.

Scientists discover mitochondria's role in reducing obesity

A stress signal received by the heart from fat could help protect against cardiac damage induced by obesity, a new study led by UT Southwestern researchers suggests.

The finding, published online in&nbsp;Cell Metabolism, might help explain the “obesity paradox,” a phenomenon where obese individuals have better short- and medium-term cardiovascular disease prognoses compared with those who are lean, but with ultimately worse long-term outcomes.

"The mechanism we have identified here could be one of many that protects the heart in obesity," said study leader Philipp E. Scherer, PhD, Professor of Internal Medicine and Cell Biology at UTSW who has long studied fat metabolism.

Study co-leader Clair Crewe, PhD, Assistant Instructor of Internal Medicine at UTSW, said the metabolic stress of obesity gradually makes fat tissue dysfunctional, causing its mitochondria — the cellular organelles that generate energy — to shrink and die. Eventually, this unhealthy fat loses the ability to store lipids generated by excess calories in food, poisoning other organs through an effect called lipotoxicity. Some organs, including the heart, appear to mount a preemptive defence to protect against lipotoxicity. But how the heart senses fat's dysfunctional state has been unknown.

In their study, Dr Crewe, Dr Scherer, and their colleagues used a genetic technique to speed the loss of mitochondrial mass and function in mice. When these animals ate a high-fat diet and became obese, the researchers found that the rodents' fat cells began sending out extracellular vesicles filled with small pieces of dying mitochondria. Some of these mitochondrial snippets travelled through the bloodstream to the heart, triggering oxidative stress, a state in which cells generate harmful free radicals.

To counteract this stress, heart cells produce a flood of protective antioxidant molecules. This protective backlash was so strong that when the scientists injected mice with extracellular vesicles filled with mitochondrial snippets and later induced a heart attack, the animals had significantly less damage to their hearts compared with mice that didn't receive an injection.

Further research using fat tissue sampled from obese patients showed that these cells also release mitochondria-filled extracellular vesicles, Dr Crewe said, suggesting that the effects observed in mice also take place in humans.

Eventually, she explained, the heart and other organs in obese individuals become overwhelmed by lipotoxic effects, leading to many of obesity's comorbidities. However, learning how to artificially generate the protective mechanism identified in this study could lead to new ways to buffer obesity's negative consequences. This knowledge could even suggest strategies to protect the heart against damage in lean individuals as well.

“By better understanding the distress signal from fat,” Dr Crewe said, “We may be able to harness the mechanism to improve heart health in obese and non-obese individuals alike.”

(With inputs from agencies)

A stress signal received by the heart from fat could help protect against cardiac damage induced by obesity, a new study led by UT Southwestern researchers suggests.

A stress signal received by the heart from fat could help protect against cardiac damage induced by obesity, a new study led by UT Southwestern researchers suggests. The finding, published online in Cell Metabolism, might help explain the “obesity paradox,” a phenomenon where obese individuals have better short- and medium-term cardiovascular disease prognoses compared with those who are lean, but with ultimately worse long-term outcomes. "The mechanism we have identified here could be one of many that protects the heart in obesity," said study leader Philipp E. Scherer, PhD, Professor of Internal Medicine and Cell Biology at UTSW who has long studied fat metabolism. Study co-leader Clair Crewe, PhD, Assistant Instructor of Internal Medicine at UTSW, said the metabolic stress of obesity gradually makes fat tissue dysfunctional, causing its mitochondria — the cellular organelles that generate energy — to shrink and die. Eventually, this unhealthy fat loses the ability to store lipids generated by excess calories in food, poisoning other organs through an effect called lipotoxicity. Some organs, including the heart, appear to mount a preemptive defence to protect against lipotoxicity. But how the heart senses fat's dysfunctional state has been unknown. In their study, Dr Crewe, Dr Scherer, and their colleagues used a genetic technique to speed the loss of mitochondrial mass and function in mice. When these animals ate a high-fat diet and became obese, the researchers found that the rodents' fat cells began sending out extracellular vesicles filled with small pieces of dying mitochondria. Some of these mitochondrial snippets travelled through the bloodstream to the heart, triggering oxidative stress, a state in which cells generate harmful free radicals. To counteract this stress, heart cells produce a flood of protective antioxidant molecules. This protective backlash was so strong that when the scientists injected mice with extracellular vesicles filled with mitochondrial snippets and later induced a heart attack, the animals had significantly less damage to their hearts compared with mice that didn't receive an injection. Further research using fat tissue sampled from obese patients showed that these cells also release mitochondria-filled extracellular vesicles, Dr Crewe said, suggesting that the effects observed in mice also take place in humans. Eventually, she explained, the heart and other organs in obese individuals become overwhelmed by lipotoxic effects, leading to many of obesity's comorbidities. However, learning how to artificially generate the protective mechanism identified in this study could lead to new ways to buffer obesity's negative consequences. This knowledge could even suggest strategies to protect the heart against damage in lean individuals as well. “By better understanding the distress signal from fat,” Dr Crewe said, “We may be able to harness the mechanism to improve heart health in obese and non-obese individuals alike.” (With inputs from agencies)

Distress signal from fat cells prompts heart to shore up defences against consequences of obesity

Britain&#39;s fertility regulator on Thursday gave the green light for the country to become the first in the world to legally offer &quot;three-parent baby&quot; fertility treatments.

British MPs had voted in February to allow the creation of in-vitro fertilisation (IVF) babies with DNA from three people, but clinics needed the approval of the Human Fertilisation and Embryology Authority before introducing the treatment.

The technique would allow women who carry disease-causing mutations in their mitochondrial genes to give birth to genetically-related children free of mitochondrial disease.

HFEA chair Sally Cheshire called the decision&nbsp;to let clinics offer mitochondrial gene therapy &quot;historic and important&quot; and &quot;a world first&quot;.

&quot;I&#39;m sure patients who might be in line for this treatment will be really pleased by what we&#39;ve decided today,&quot; she said, but added: &quot;We will proceed with caution.&quot;

An independent panel of experts last month said the practice should be &quot;cautiously adopted&quot; to prevent certain genetic diseases from being passed on to future generations.

Mitochondria are structures in cells which generate vital energy and contain their own set of genes called mDNA which is passed through the mother.

Mitochondrial diseases cause symptoms ranging from poor vision to diabetes and muscle wasting and health officials estimate around 125 babies are born with the mutations in Britain every year.

(AFP)

The process would allow women carrying disease-causing mutations in their genes to give birth to genetically-related children free of disease

Britain's fertility regulator on Thursday gave the green light for the country to become the first in the world to legally offer "three-parent baby" fertility treatments. British MPs had voted in February to allow the creation of in-vitro fertilisation (IVF) babies with DNA from three people, but clinics needed the approval of the Human Fertilisation and Embryology Authority before introducing the treatment. The technique would allow women who carry disease-causing mutations in their mitochondrial genes to give birth to genetically-related children free of mitochondrial disease. HFEA chair Sally Cheshire called the decision to let clinics offer mitochondrial gene therapy "historic and important" and "a world first". "I'm sure patients who might be in line for this treatment will be really pleased by what we've decided today," she said, but added: "We will proceed with caution." An independent panel of experts last month said the practice should be "cautiously adopted" to prevent certain genetic diseases from being passed on to future generations. Mitochondria are structures in cells which generate vital energy and contain their own set of genes called mDNA which is passed through the mother. Mitochondrial diseases cause symptoms ranging from poor vision to diabetes and muscle wasting and health officials estimate around 125 babies are born with the mutations in Britain every year. (AFP)

UK approves 'three-parent' gene therapy