By Claire Kowalick<\/p>\n
Obesity is increasing in children and adolescents at an alarming rate, and scientists are only beginning to understand its effect on these children\u2019s future health. Between 2017 and 2020, youth obesity in the United States increased by nearly 20%, now affecting nearly 15 million children, according to the Centers for Disease Control and Prevention. In South Texas, the rates are even higher \u2014 ranging from 25% to 31% in some youth populations.<\/p>\n
While public awareness of obesity has expanded considerably over the past decade, the fundamental biological underpinnings of the disease, especially in children, remain poorly understood. Researchers at The University of Texas at San Antonio’s Health Science Center are among a growing number of scientists working to uncover the unique biology of childhood obesity. Their goal is to pave the way for targeted prevention and treatment strategies that can reverse this dangerous trend.<\/p>\n
One key insight from emerging research is that childhood obesity is not simply adult obesity occurring earlier. The disease behaves differently in children, presenting unique biological and developmental challenges.<\/p>\n
\u201cObesity is a dynamic condition influenced by nutrition and hormones, but in children it exhibits distinct characteristics and critical windows during development,\u201d said Lily Dong, PhD, professor and chair of the Department of Cell Systems and Anatomy at the Health Science Center and an investigator in childhood obesity research.<\/p>\n
Dong began her career studying DNA replication and gene regulation, but after moving to San Antonio nearly 30 years ago, she shifted her focus to metabolic dysfunction. She was driven by the stark health disparities she observed in South Texas, where obesity-related diseases were taking a heavy toll.<\/p>\n
In adults, obesity is commonly linked with elevated blood glucose, insulin resistance and chronic inflammation. Children, however, may show high insulin levels while maintaining normal blood sugar, a subtle but important distinction that suggests internal dysfunction begins before full-blown metabolic disease manifests.<\/p>\n
Puberty adds another layer of complexity. As children grow, their fat storage shifts in type, function and distribution. For instance, infants are born with abundant brown adipose tissue and subcutaneous fat, which are protective and energy rich. As they move into adolescence, hormonal changes influence how fat is stored. When caloric intake exceeds the body\u2019s needs, known as overnutrition, visceral fat \u2014 a harmful type that surrounds internal organs \u2014 accumulates and drives chronic, low-grade inflammation.<\/p>\n
\u201cIt took decades of advocacy and science for adult obesity to be recognized and treated seriously. We must do the same for children \u2014 but move faster. Scientists, clinicians and society must work together. My dream is that one day, childhood obesity rates will start to fall. But that will only happen if we act now.\u201d<\/span><\/p><\/blockquote>\n
\u2013 Lily Dong, PhD<\/strong>, professor and chair of the Department of Cell Systems and Anatomy<\/span><\/h6>\n
Hormonal drivers of childhood obesity<\/span><\/strong><\/h3>\n
A major focus of Dong\u2019s research is on adipokines \u2014 hormones secreted by adipocytes, or fat cells, which regulate energy balance. These molecules act as both sensors and regulators of the body\u2019s metabolic state. However, with chronic overnutrition this regulatory system begins to fail.<\/p>\n
Her lab identified a novel adipokine called leucine-rich alpha-2-glycoprotein 1 (LRG1), as reported in The Journal of Clinical Investigation. LRG1 levels rise in response to overnutrition and contribute to fatty liver disease and obesity. A more recent study from her group, published in Diabetologia, showed that elevated LRG1 can also stimulate insulin release from the pancreas, leading to hyperinsulinemia \u2014 a key contributor to visceral fat accumulation.<\/p>\n
Now, Dong\u2019s lab is investigating LRG1\u2019s role in children, where it may have developmental stage-specific effects.<\/p>\n
\u201cOur unpublished data indicate that LRG1 seems to serve different roles depending on age,\u201d Dong said. \u201cIn children, we suspect that its dysregulation disrupts leptin signaling \u2014 the key hormonal pathway that tells the brain when to stop eating.\u201d<\/p>\n
The leptin paradox<\/strong><\/span><\/h3>\n
Leptin is the hormone responsible for signaling satiety. When energy stores are sufficient, leptin tells the brain to reduce appetite. However, many adolescents with obesity have elevated leptin levels, suggesting the signal is being sent but ignored \u2014 a condition known as leptin resistance. This malfunction perpetuates overeating despite abundant fat reserves.<\/p>\n
\u201cThis is one of the defining features of childhood obesity,\u201d Dong said. \u201cThese kids have plenty of leptin, but their brains aren\u2019t responding.\u201d<\/p>\n
The narrow developmental window of adolescence leaves little room for error. Hormonal shifts, nutritional factors and genetic predispositions converge during this critical period. Since children are still growing, interventions must be carefully tailored to avoid disrupting normal development.<\/p>\n
Environmental factors, especially diet, play a profound role. Dong\u2019s team uses animal models to study how overnutrition alters metabolism at different life stages. Their aim is to pinpoint when obesity transitions from a reversible condition to a progressive disease.<\/p>\n
\u201cThere is a window where we may still be able to reverse the damage,\u201d Dong notes. \u201cOnce that window closes, the risk of complications like cardiovascular disease, kidney failure and [pancreatic] beta cell dysfunction rise sharply.\u201d<\/p>\n
Targeted treatments<\/strong><\/span><\/h3>\n
Currently, there are only a few U.S. Food and Drug Administration-approved treatments for childhood obesity, most of which are adaptations of medications originally developed for adults. Dong\u2019s lab aims to develop therapies specifically designed for children, grounded in a deeper understanding of their unique biology.<\/p>\n
They are investigating the use of neutralizing antibodies or small peptides to restore hormonal balance and are also exploring the development of biomarker-based tests, via blood or urine, to detect early signs of metabolic dysfunction.<\/p>\n
One of the greatest challenges, Dong emphasizes, is designing interventions that adapt to the evolving physiology of growing children.<\/p>\n
“We want to tailor the hormonal response to match each developmental stage,” she said. \u201cDesigning effective therapies for youth is difficult, but critically important. The problem is accelerating faster than science can respond.\u201d<\/p>\n
An urgent call to action<\/strong><\/span><\/h3>\n
Obesity was officially recognized as a disease by the American Medical Association in 2013. Research into adolescent obesity is an even more recent focus, and major gaps in understanding remain.<\/p>\n
\u201cThis is a chronic disease that develops over years and can lead to irreversible metabolic dysfunction,\u201d Dong said. \u201cBut the rates are rising at an alarming pace \u2014 we don\u2019t have the luxury of time.\u201d<\/p>\n
Despite the challenges, Dong remains optimistic.<\/p>\n
\u201cIt took decades of advocacy and science for adult obesity to be recognized and treated seriously,\u201d she reflected. \u201cWe must do the same for children \u2014 but move faster. Scientists, clinicians and society must work together. My dream is that one day, childhood obesity rates will start to fall. But that will only happen if we act now.\u201d<\/p>\n
\nChildhood obesity is associated with elevated insulin and inflammatory proteins in the blood<\/strong><\/span><\/h2>\n
Hyperinsulinemia, or elevated insulin in the blood, is a known predisposing factor for insulin resistance and the development of Type 2 diabetes. In a recent mouse model study, Dong\u2019s lab demonstrated that LRG1, a protein that increases during inflammation, caused pancreatic beta cells to release too much insulin. The protein caused the endoplasmic reticulum, a cell\u2019s storage center, to release extra calcium, which then signals a release of insulin, even if glucose is not present. The findings suggest that higher levels of LRG1 could serve as both a biomarker and potential therapeutic target for early detection and intervention of hyperinsulinemia in childhood obesity and Type 2 diabetes.<\/p>\n","protected":false},"excerpt":{"rendered":"
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