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Some 20 percent of cancer-related deaths in the U.S. can be attributed to obesity, making it the number-one preventable cause of cancer death in the country. But with myriad metabolic and inflammatory changes associated with obesity, determining the mechanisms that underlie the obesity-cancer link has proven challenging.

This case study was developed for an introductory biology course with the goal of integrating content (specifically, structure/function, signaling pathways, and homeostasis) while reinforcing general critical thinking skills and the scientific method (generating hypotheses, evaluating evidence, and making predictions). The case is suitable for a flipped classroom and there are several videos associated with it. The case revolves around an obese two-and-a-half-year-old boy who won't stop eating. Students become familiar with some basic concepts related to obesity and leptin signaling through the videos that they watch before class. They then use class time to work through the case (delivered as an interactive slide show, including several clicker questions) to determine the genetic basis for this child's obesity and possible therapies to manage his weight. The case could also be adapted and expanded to be used in a physiology course to explore the interaction of various hormones that regulate appetite and metabolic rate or in a cell biology class to explore JAK-STAT signaling.

In our view, and that of organizations such as the American Society of Clinical Oncology, the World Cancer Research Fund International, and the American Cancer Society, obesity-related cancers will arguably be the most urgent issue in the cancer field in the next decade.

"There has been an over-reliance on male animals in preclinical research in the past, and as we have worked to study female specific physiological conditions, we became aware that even many aspects of our basic model of diet induced obesity are different in females," Erin Giles, assistant professor at Texas A&M University and lead author of the study, said in a press release.

Of two genetically identical mice, how can one be small and another fat? Research on epigenetic changes resulting from the environment can give us clues into obesity in mice--and humans.

The laboratory-based animal study found a link between greater susceptibility to obesity and diabetes, and whether one's ancestors have been undernourished for several generations, and was published on Friday in the journal Cell Metabolism.

In 2007, researchers discovered that people with a common variant of FTO tend to be heavier than those without it. Since then, studies have repeatedly confirmed the link. On average, one copy of the risky variant adds up to 3.5 extra pounds of weight. Two copies of the gene bring 7 extra pounds - and increase a person's risk of becoming obese by 50 percent.

Mouse study fingers potential cause of fertility problems, proposing obesity and egg quality link.

Gut microbes-the collection of bacteria and other organisms that inhabit our intestines-have been shown to play a role in a wide variety of conditions from asthma to obesity. But researchers still don't know precisely how they contribute to obesity. To gain a better understanding, a team led by physiologist Mirko Trajkovski from the University of Geneva in Switzerland has been following up on any leads he can to learn about the link between these microbes and metabolism. Trajkovski knew from past research that getting rid of some gut bacteria in mice makes them less able to maintain their internal body temperature in the cold. He wondered whether there might be a connection between gut microbes, external temperature, and weight control.

This "clicker case" tells the story of "Hannah," a baby girl adopted by two loving parents who grows up with an uncontrolled appetite and develops severe early-onset obesity. Students follow Hannah's story as she develops excessive eating early in life, which her health care team is unable to explain. A visit to obesity specialists finally reveals the underlying cause of Hannah's obsession with food: extremely low levels of circulating leptin, a hormone that regulates appetite and body weight. It is further discovered that Hannah's leptin deficiency is due to a mutation in the LEP gene. As the story unfolds, students first work on unit conversions and BMI calculations to practice quantitative skills as well as graph and data interpretation skills. Students then apply their knowledge of DNA transcription, translation, and protein structure to answer questions based on figures from a 2019 study on LEP mutations. The case is best suited for high school and lower-level undergraduate biology courses.

Researchers from the World Health Organization's International Agency for Research on Cancer (IARC) looked at more than 1,000 epidemiological studies and found that "excess body fatness" is also linked to the risk of developing gastric, liver, gallbladder, pancreatic, ovarian, thyroid, blood (multiple myeloma) and brain (meningioma) cancers.

Children with obese fathers have different epigenetic markings on the gene for insulin-type growth factor 2 (IGF2)-which is important during fetal growth and development-than children with fathers of normal weight.

IN recent weeks, two major medical organizations have issued independent warnings about toxic chemicals in products all around us. Unregulated substances, they say, are sometimes linked to breast and prostate cancer, genital deformities, obesity, diabetes and infertility. "Widespread exposure to toxic environmental chemicals threatens healthy human reproduction," the International Federation of Gynecology and Obstetrics warned in a landmark statement last month.

Men, your sperm know how heavy you are. A new study reveals that sperm carry different chemical tags on their DNA depending on whether their owner is lean or obese. The findings suggest that men may be able to pass information about the availability of food in their environment down to their offspring, which could influence their child's odds of being overweight.

Our bodies are home to approximately 100 trillion bacteria living inside us and on us-a vast community known as the microbiome. The Secret World Inside You explores the rapidly evolving science that is revealing the complexities of the human microbiome and reshaping our ideas about human health, offering new perspectives on common health problems including allergies, asthma, and obesity. 

Life on Earth is intimately connected to the natural cycles of light and dark that make up a 24-hour day. For plants, animals, and even bacteria, these circadian rhythms control many biological functions. Humans can overrule their body clocks, but at a price: People whose circadian rhythms are regularly disrupted-by frequent jet lag or shift work, for example-are more vulnerable to diabetes, obesity, cardiovascular disease, and cancer. There are various theories to explain these associations, and researchers now have a new player to consider: the bacteria that live in the digestive tract. According to a study in mice and a small group of human volunteers, the internal clocks of these gut microbes sync up with the clocks of their hosts. When our circadian rhythms get out of whack, so do those of our bacteria.

Scientists work with animal models to better understand type 2 diabetes to treat the disease. They have developed specialized animal models that mimic the condition.  One line of mice, known as KK mice, develop obesity and glucose intolerance that lead to type 2 diabetes. Another rodent model, the Zucker diabetic fatty rat, is bred to be a precise model of human type 2 diabetes.

"Millions of people who suffer from less-intense sleep problems do suffer myriad health burdens. In addition to emotional distress and cognitive impairments, these can include high blood pressure, obesity, and metabolic syndrome. And recent research has suggested even mild sleep loss, the kind people often subject themselves to during the work week by watching late-night TV until midnight then rising before dawn, may lead to metabolic, cardiovascular, cognitive, and neurologic dysfunction."

Health care costs have been a hot button topic in recent years, and rightfully so. The United States spends an extraordinary amount of money on health care each year - $9,523 for every man, woman and child to be exact. This totals over 1 trillion dollars, accounting for roughly 17 percent of the United States' gross domestic product (GDP). The federal government spends 27 percent of its total budget on health care. Astonishingly more than it spends on the military, food and agriculture, education, transportation, and international affairs combined. So where is all the money going? Strangely enough, to combat just a few diseases.

Women who are overweight while pregnant are more likely to have babies who are biologically older than those born to women of a healthy weight. This could put the babies at a higher risk of developing chronic diseases later in life, and may reduce their life expectancy. Our biological age is linked to the length of our telomeres - bits of DNA that cap the ends of our chromosomes. Our telomeres shrink every time our cells divide, and continue to shorten throughout life. "Short telomeres have been associated with cardiovascular disease, type 2 diabetes and atherosclerosis," says Tim Nawrot at Hasselt University in Belgium.