According to the US Centers for Disease Control and Preventionthe prevalence of metabolic syndrome, which places people at significantly higher risk of diabetes, heart disease, and stroke, is about 34.2% in US adults. The typical treatment is a healthy diet, exercise, and possibly metformin to control blood sugar. There may be a new treatment on the horizon. For that and more research news, continue reading.
A Potential New Treatment for Metabolic Syndrome
Metabolic syndrome is associated with a greater risk of diabetes, heart disease and stroke. Part of the syndrome includes obesity, high blood pressure and high blood sugar. Researchers at the University Hospitals Cleveland Medical Center, working on a mouse model, developed a drug to treat metabolic syndrome by identifying a receptor that controls appetite and body weight. They discovered a hormone in 2016 called asprosin, which stimulates appetite and increases glucose levels. It does this by acting on the hypothalamus and the liver. People with low blood asprosin levels don’t feel hunger like other people and have lower glucose and insulin levels. It stimulates appetite by activating hunger neurons called AgRP neurons.
“By using a sophisticated technique called mass spectrometry, we identified protein tyrosine phosphatase receptor (Ptprd) as the receptor for asprosin,” said Ila Mishra, Ph.D., first author of the study and research associate at Harrington Discovery Institute and Case Western Reserve School of Medicine. “Genetic deletion of Ptprd in mice reduced appetite and body weight, rendering mice unresponsive to asprosin’s appetite-stimulating effect. In other words, Ptprd is necessary for asprosin-mediated appetite stimulation. This result is the crux of our discovery. A receptor is necessary for a hormone to work, and in the case of asprosin’s ability to control appetite and body weight, that receptor is Ptprd.”
They used the discovery of the receptor to develop a new drug they call a receptor trap. It suppresses appetite, body weight and blood glucose levels in obese mice by sequestering plasma asprosin. This could potentially become a new drug against metabolic syndrome.
NK Cells with Bispecific Antibody Effective for Lymphoma
Investigators with The University of Texas MD Anderson Cancer Center demonstrated that natural killer (NK) derived cells from donated umbilical cord blood combined with a novel bispecific antibody that targets CD16A and CD30 have effective responses in pretreated and refractory CD30+ lymphoma. The antibody is called AFM13. The treatment reported an 89% overall response rate (ORR) in 19 patients, with 10 complete responses (CR). Progression free survival (PFS) and overall survival (OS) rates for all three doses were 52% and 81%, respectively, after 11 months of median follow-up and a lead-in follow-up of 19 months. The antibody was developed by biotech company Affimed.
Certain Personality Traits Associated with Cognitive Functioning Late in Life
Researchers at the University of Victoria published research that associated certain personality traits with cognitive function later in life. Generally, they found that people with high levels of self-discipline who are organized are possibly less likely to develop mild cognitive impairment as they age. People who are generally moody or emotionally unstable are more likely to experience cognitive decline. The focus was on what they called three of the “Big Five” personality traits: conscientiousness, neuroticism and extraversion. People high in conscientiousness tend to be responsible, organized, hard-working and goal-directed. People high on neuroticism have lower emotional stability with a tendency toward mood swings, anxiety, depression and self-doubt. Extraverts gain energy from being around other people and are generally enthusiastic, outgoing, talkative and assertive. The study was based on data from 1,954 participants in the Rush Memory and Aging Project.
How to Rejuvenate the Immune System of the Elderly
Scientists with the University of California, Irvine identified a reason older adults are more susceptible to infectious diseases than younger people. The research is associated with age-associated impairment of T cells and the finding that branched glycans increase with age in T cells from females more than in males. These glycans suppress T cell function. These age-related glycans appear to be related to increases in a sugar metabolite, N-acetylglucosamine, and signaling by the T cell cytokine interleukin-7. In a mouse model, reversing elevation of branched glycans rejuvenated human and mouse T cell function and decreased the severity of Salmonella infection in old female mice.
Smoking and Lung Cancer—Another Puzzle Piece
Smoking cigarettes is overwhelmingly associated with lung cancer. However, only a minority of smokers develop lung cancer. Researchers at Albert Einstein College of Medicine found evidence that some smokers have genetic mechanisms that protect them from lung cancer by limiting mutations. Mutations also accumulate in the lungs of non-smokers, but many more in smokers. Very few non-smokers get lung cancer, but about 10% to 20% of lifelong smokers do. The researchers developed a new sequencing technique called single-cell multiple displacement amplification (SCMDA), which allowed them to compare the mutational landscape of normal lung epithelial cells in never-smokers, smokers, and heavy, long-term smokers. They found significantly more mutations in the lung cells of smokers. They also found that the mutations detected in lung cells increased in a straight line with the number of “pack years” of smoking the people did, suggesting that the longer you smoke, the greater the risk of lung cancer, although it appears to halt after 23 pack years of exposure. They theorize this is because these people have a mechanism that suppresses further mutation accumulation.
“The heaviest smokers did not have the highest mutation burden,” said Dr. Simon Spivack, MD, MPH, co-senior author of the study and a professor of medicine, epidemiology & population health, and of genetics at Einstein, and a pulmonologist at Montefiore Health System. “Our data suggest that these individuals may have survived for so long in spite of their heavy smoking because they managed to suppress further mutation accumulation. This leveling off of mutations could stem from these people having very proficient systems for repairing DNA damage or detoxifying cigarette smoke.”