Obese mice lost their ability to taste sweets, which, conceivably, played a role in their desire for food. Also this week: a vaccine approach to high blood pressure and a smoother path to spinal cord repair.
Obesity A Taste-Bud Killer?
The population of taste-receptor cells responsive to sweets decreased significantly in mice with diet-induced obesity.
Compared with normal-weight animals, obese mice had about a third as many receptor cells that responded to the artificial sweeteners saccharin (P<0.001) and acesulfame K (P<0.01). The loss of sweet-responsive cells was associated with altered taste-evoked calcium signaling, which was used to measure the cells' response to different taste stimuli.
"If we understand how these taste cells are affected and how we can get these cells back to normal, it could lead to new treatments [for obesity]," Kathryn Medler, PhD, of the University at Buffalo in New York, said in a statement. "These cells are out on your tongue and are more accessible than cells in other parts of your body, like your brain."
-- Charles Bankhead
An Antihypertensive Vaccine?
Vaccination against the pressure-raising hormone angiotensin II lowered blood pressure in rats for up to 6 months, researchers reported at the American Heart Association meeting in Dallas.
The DNA vaccine stimulated antibodies specific to angiotensin I and II and produced a 33 mm Hg decrease in systolic pressure compared with unvaccinated rats that persisted at least 6 months. It also cut cardiac and blood vessel damage associated with high blood pressure, without any autoimmune reaction observed.
While anti-angiotensin II blood pressure pills are already widely used, the vaccine could get around adherence problems that leave patients at elevated risk of stroke and other cardiovascular events.
"Future development of DNA vaccine to hypertension may provide a new therapeutic option to treat hypertensive population," Hiroshi Koriyama, MD, of Japan's Osaka University, and colleagues concluded.
-- Crystal Phend
Injured Mouse Spine Recovers With Stem Cells
Neither the injection point nor the dose of neural stem progenitor cells for spinal cord injury repair made a difference in outcomes, according to a preclinical study by Japanese researchers reported in Cell Transplantation.
Clinical development of stem cell transplantation for spine injury is underway, but the ideal quantity of cells and graft site have not yet been identified, so researchers led by Masaya Nakamura, MD, PhD, conducted a series of experiments using bioluminescent neural stem progenitor cells from fetal transgenic mice.
They demonstrated that both low and high doses of the cells led to motor recovery. They also determined that expression of brain-derived neurotrophic factor was higher in the adjacent sites, where differentiation into neurons was greater than into astrocytes. Also, the microenvironments of both inter-lesional and adjacent transplant sites successfully supported the engrafted cells.
Nevertheless, the researchers concluded that at least some cells should be delivered directly into the lesion during the subacute phase of injury, to prevent any potential further damage to intact adjacent areas of the spine.
-- Nancy Walsh
Cold Mice = Bad Medicine?
Research into cancer immunotherapies may have been hindered by keeping research animals at the wrong temperature, a new study suggested.
Lab mice are generally happiest at temperatures of about 30 °C, but their human keepers prefer temperatures a bit cooler, in the 20° to 26 °C range. This creates "mild chronic cold stress" in the mice, according to Elizabeth Rapasky, PhD, of Roswell Park Cancer Institute in Buffalo, N.Y., and colleagues, writing in Proceedings of the National Academy of Sciences. That forces the animals to crank up their metabolic machinery to maintain their body temperature.
Rapasky and colleagues examined the effect of temperature on tumor genesis, growth, and spread in mice kept at different temperatures. They found that, at the animals' preferred temperature, anti-tumor immune activity was markedly greater than when they were housed in the cooler environment, and tumor growth was suppressed.
"Our data raise the hypothesis that suppression of anti-tumor immunity is an outcome of cold stress-induced thermogenesis," the researchers wrote. In turn, this effect may mask "the full potential of the anti-tumor immune response" that might otherwise be seen in preclinical studies.
-- John Gever