Month: March 2025

Rates of obesity and overweight are spiralling due to a “monumental societal failure” to tackle the problem, with more than half of adults and almost a third of children and young people set to be affected by 2050, according to a new study published in The Lancet. That represents more than 3.8 billion adults and 746 million children and adolescents. As we commemorate World Obesity Day, FRANCE 24’s Genie Godula welcomes Dr. Karen Coulman, Senior Research Fellow and Obesity Specialist Dietitian at the University of Bristol.
#Health #Obesity #WorldObesityDay

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Hyderabad: Healthcare experts on Tuesday called on people to curtail sugar in-take to fight obesity as a study conducted by AIG Hospitals found that 80 per cent of IT professionals in Hitec City were overweight.
AIG Hospitals also announced the launch of a dedicated website for its Centre for Obesity and Metabolic Therapy, providing expert consultations and treatment information.
Speaking at a panel discussion organised by AIG Hospitals on the health risk caused by obesity, Dr Ramakrishna said: “In order to reduce weight, cutting down on sugars is essential. About 10-20 per cent reduction in weight can be seen if we stop eating sugars. It also helps prevent cardiovascular diseases. This includes all kinds of sugars, brown, jaggery, and artificial sweeteners.”
The panel discussion was organised on the occasion of World Obesity Day.
With obesity being tagged as an epidemic and a multifactorial disease impacting all bodily functions, doctors talked about the causes, prevention, management and treatment of obesity. The panel featured specialists from gastroenterology, cardiology, pulmonology, psychology and others.
“The impact of obesity on lungs is huge as it increases the risk of immune disregulation. Obese people are more at risk of getting pneumonia, influenza, and other infections. The rate of mortality increased among obese people who get these diseases, as observed during Covid period,” said Dr Vishwanath.
People with obesity also deal with sleep problems. With fat deposited in lungs and neck, people are unable to breathe while sleeping. With abdominal fat, the diaphragm is unable to move. It also causes a cascade of inflammatory problems. Therefore, it is important to get 6-8 hours of deep sleep.
Doctors also mentioned that obese people are more predisposed to get cancers. Additionally, 40 per cent of children in government schools have non-alcoholic fatty liver disease (NAFLD), highlighting the urgency of action.
Maintaining a healthy, balanced diet is key to avoiding obesity and related diseases. Doctors mentioned that intermittent fasting, where people can have proper health meals during 8 hours in the day and then not eat anything for the next 16 hours, works better than fasting on alternate days.
A major discrepancy in nutrition is lack of fruits and vegetables in the Indian diet. While the recommendation is 500 gm of vegetables per day, an individual only consumes 50 gms of vegetables per day. Not knowing what to eat, people just end up going hungry to avoid gaining weight and lose out on nutrition as well.
The human body also needs at least one gram of protein per kilogram of body weight. The psychological aspect of obesity is that most people are surrounded by a toxic food environment, where junk food is easily available and is encouraged. Avoiding such exposure is necessary.
Hyderabad police commissioner C.V. Anand stressed that obesity is influenced by more than just food choices. He also launched FitCop, an app with 18,000 enrolled officers. The initiative identified 300-400 officers at risk for lifestyle diseases.

Worldwide obesity rates have more than doubled since 1990, with nearly a billion people now falling into the category. Though a complex interplay of genes, diet, and environment contribute, 90% of cases have leptin resistance in common.
In lean individuals, fat cells produce the hormone leptin, which suppresses appetite. But in most individuals with obesity, this signal fails to register. Why this happens has been a mystery for more than three decades, ever since Jeffrey M. Friedman’s laboratory at the Rockefeller University cloned the leptin gene in 1994.

But now Friedman, MD, PhD, together with Bowen Tan, Kristina Hedbacker, PhD, and other researchers in Friedman’s Laboratory of Molecular Genetics have discovered a neural mechanism involved in leptin resistance, and identified a way to reverse it in mice using the mTOR inhibitor rapamycin. The team found that rapamycin restores leptin sensitivity to diet-induced obese (DIO) mice, leading to significant loss of fat with only minimal effects on muscle.
“Before our research, the cause of obesity in diet-induced obese mice was unknown, leaving a critical gap in our understanding of how leptin resistance develops and how it can be reversed,” said Tan, a graduate student in Friedman’s lab. “Even though Jeff Friedman discovered this powerful hormone back in 1994, its full potential to help people lose weight hasn’t been realized because most obese patients have acquired resistance to leptin,” added Hedbacker, a research specialist at Howard Hughes Medical Institute and a member of Friedman’s lab. “It’s really exciting to think that there may be means for addressing this.”
Senior author Friedman, together with co-first authors Tan, Hedbacker, and colleagues reported on their work in Cell Metabolism, in a paper titled, “A cellular and molecular basis of leptin resistance,” in which they suggest their findings establish “.. a key pathogenic mechanism leading to obesity.”

“Obesity is the cardinal feature of metabolic syndrome and a worldwide public health problem,” the authors wrote. Long before plant agriculture and animal domestication provided more reliable access to nutrients, humans routinely faced starvation. That’s when the leptin circuit evolved. Neurons in the hypothalamus—the brain’s energy-balance regulator—pick up satiety signals from fat, which secretes leptin. A high amount of the hormone signals that there are adequate fat stores and the energy tank is full, while a low leptin level indicates that the body is running on fumes. “In lean animals, adipose tissue mass is tightly controlled by the hormone leptin (LEP), which functions as the afferent signal in a negative feedback loop that maintains energy balance,” the authors explained. “LEP reduces appetite, in part by activating α-MSH (POMC)-expressing neurons in the arcuate nucleus (ARC) of the hypothalamus.”
Our brains retain this system for regulating food consumption, even as conditions around it have drastically changed, with more people having access to high-calorie foods than ever before. Data suggest that as weight is gained and leptin levels continually rise, the brain gradually stops responding to leptin. “This phenomenon is analogous to insulin resistance, which is the most common cause of diabetes and a condition that develops over time, due, in part, to chronically elevated insulin levels,” Hedbacker said. “Similarly, most people with obesity have high leptin, but reception of their leptin signaling is blocked. This makes it very difficult to lose weight because the brain does not receive the appropriate signal of how much fat is stored.”
With this in mind, Tan and Hedbacker set out to identify biomarkers in the 10% of patients with obesity who are leptin-sensitive and could potentially benefit from leptin treatment. They looked at both leptin-sensitive and leptin-resistant mice. “Similar to most humans with obesity, diet-induced obese (DIO) mice have high leptin levels and fail to respond to the exogenous hormone, suggesting that their obesity is caused by leptin resistance, the pathogenesis of which is unknown,” the authors noted.
What they discovered sent them down an unexpected path. The scientists found that in leptin-resistant mice, the levels of two essential amino acids are dysregulated in response to leptin. These two amino acids, methionine and leucine, are known activators of a signaling molecule called mTOR (mammalian target of rapamycin). Leptin-sensitive animals showed no such dysregulation.
“With this as a starting point, we found that mTOR is hyperactive in specific brain regions and cell types in obese animals,” Tan said. For their study the researchers tested the effects of the mTOR inhibitor rapamycin in four groups of mice: leptin-sensitive mice fed a low-calorie chow diet, mimicking people who remain lean; mice fed a high-fat diet that developed leptin resistance, similar to people who develop obesity; and two sets of obese mice that were leptin-deficient but responsive to the hormone. These mice were fed either the low-calorie chow diet or the high-fat diet. “Our finding that LEP sensitivity was inversely associated with plasma levels of mTOR activators led us to hypothesize that mTOR activation might diminish LEP sensitivity in DIO mice. We evaluated this possibility by treating DIO mice with rapamycin (RAP), a specific mTOR inhibitor,” they explained.
The results were striking: “Obese mice fed a high-fat diet and treated with the mTOR inhibitor rapamycin lost significant amounts of weight, which—similar to leptin treatment in leptin-sensitive animals—was primarily due to a decrease in the amount of adipose tissue,” Tan said. The authors further noted, “We found that RAP, a specific mTOR inhibitor, reduces body weight in DIO mice but not in mice with defects in LEP signaling or low circulating levels of the hormone.”

The team then investigated which cell types in the brain were the target of rapamycin, focusing on a dozen cell types in the hypothalamus, where leptin is known to act. Using single-cell sequencing, Tan found that rapamycin treatment exerted significant effects on neurons in the hypothalamus that express a gene known as POMC. These neurons are known to mediate leptin’s weight-reducing effects. “We then employed snRNA-seq to show that RAP treatment of DIO, but not lean mice, specifically induced gene expression in POMC neurons that promote LEP signaling and melanocortin production,” they wrote. “Further studies showed that POMC neurons and melanocortin signaling are necessary for RAP’s weight-reducing effects and that increased mTOR activity in POMC neurons is sufficient to cause LEP resistance.”
Added Hedbacker, “We found that rapamycin reduced mTOR in POMC neurons and restored their receptivity, essentially resensitizing the animals to leptin and leading to a decreased size of fat depots relative to muscle mass.” Defects in POMC-expressing neurons are also known to cause leptin resistance and obesity, Friedman noted, adding, “it was satisfying to find that an acquired form of leptin resistance targets this same pathway.”
By showing that it is possible to restore leptin signaling, the findings could potentially lead to new obesity treatments. “In summary, we show that LEP resistance in DIO animals is caused by increased mTOR activity in POMC neurons and that RAP reduces obesity by re-sensitizing endogenous LEP signaling in these cells,” the authors wrote. “These findings thus have important implications for our understanding of the pathogenesis of obesity and potential therapeutic applications.”
Loss of fat mass without muscle mass is characteristic of leptin treatment, but it’s unusual for weight loss in general. For example, weight loss achieved by dieting or treatment with highly effective anti-obesity medications such as Ozempic leads to a significant loss of both fat and muscle. “Reversing LEP resistance could also have clinical implications, particularly because LEP spares lean body mass in contrast to the new peptide-based therapeutics that can cause significant loss of lean mass,” the scientists pointed out.
Future research in Friedman’s lab will explore why a high-fat diet elevates mTOR signaling in the brain. The lab will also try to develop means for inhibiting mTOR specifically in POMC neurons to avoid potential side effects of systemic rapamycin use, which is linked to glucose intolerance and potentially diabetes.
“The development of brain-specific rapalogs provides a possible means to selectively reduce mTOR activity in the brain, and it might also be possible to develop cell-specific mTOR modulators,” the investigators noted. “Alternatively, the development of means for cell-specific delivery of RAP to POMC neurons could provide new avenues for treating obesity or maintaining weight loss.”
The post Rapamycin Restores Leptin Sensitivity and Leads to Fat Loss in Obese Mice appeared first on GEN – Genetic Engineering and Biotechnology News.

We present this special focus issue on March 4th, coinciding with World Obesity Day 2025, to show our solidarity with the World Obesity Federation and advocate for increased awareness, prevention, and treatment of obesity. We embrace this year’s World Obesity Day theme, “Changing Systems,” which challenges us to broaden our perspective from viewing obesity as solely an individual issue and recognize the wider systemic factors that contribute to the rapidly escalating rates of obesity worldwide. As researchers and as editors we often take a narrow view, focusing on specific genes, molecules, or cell signaling pathways that impact metabolism and contribute to obesity. However, with this issue, we aim to expand that view, presenting papers that highlight how body systems cooperate to impact metabolic health and, more broadly, how environmental factors, including food systems, contribute to this complex disease. By understanding the systems that influence obesity on a broader level, we can hope to optimize current disease management and to uncover novel approaches to combat it.

Obesity is a growing public health issue that has recently been transformed through the advent of new medicines. However, our understanding of the pathways and mechanisms that regulate energy balance in mammals is still developing. Recent discoveries on this front include an exciting new finding that there exists a novel class of metabolites in humans and mice that can regulate obesity in rodents.

Rates of obesity and overweight are spiralling due to a “monumental societal failure” to tackle the problem, with more than half of adults and almost a third of children and… Reuters Health Information

Obesity rates are set to skyrocket, with one in six children and adolescents worldwide forecast to be obese by 2050, according to a new study. But with significant increases predicted within the next five years, the researchers stress urgent action now could turn the tide on the public health crisis.

On World Obesity Day, the public health doctor says while much is changing around drugs and weight loss, we cannot lose sight of the need for access to affordable, healthy foods.