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A chemical thermostat for fat?

A chemical thermostat for fat?

Enticed by theories that there arechemicals in the body that work as a thermostat and signal a satisfied appetite, scientists have been searching for these "adipostats,' hoping to better understand and treat the different types of obesity. After finding abnormal levels of a substance called adipsin in overweight rodents, researchers in Boston said last week that adipsin may be a contender for the adipostat title, as well as a marker to differentiate among obesities due to defects in genes, metabolism or just plain will power.

Reported in the July 24 SCIENCE, experimentsby scientists at Beth Israel Hospital and Harvard Medical School showed that adipsin is primarily found in adipose tissue (fat), is carried in the bloodstream and is produced in abnormal levels in certain types of obesity. In earlier reports, the Boston group had described adipsin as a substance--probably an enzyme--secreted by fact cells.

To determine adipsin levels in differenttissues, the scientists measured the messenger RNA (mRNA) responsible for adipsin production, finding that some obesity syndromes "are associated with profoundly reduced expression of adipsin mRNA and circulating adipsin protein.' For example, adipsin mRNA levels in two different mouse models were at least 100-fold lower than those in normal controls. Victims of defective genes, both groups of mice become grossly overweight soon after birth, and have blood sugar and insulin imbalances. Adipsin itself is "radically reduced' in their serum and "virtually undetectable' in their fat tissue, say the scientists.

Suppressed mRNA levels also occurredin animals with chemically induced obesity. Those experiments used mice injected with large amounts of monosodium glutamate (MSG), causing impaired energy utilization and obesity despite a normal appetite. The scientists say these data represent one of the first examples of obesity related to abnormal gene expression. They also suggest that some aspects of obesity may be caused by adipsin deficiency, not by overeating.

But there apparently is no adipsin-basedexcuse for the can't-say-no crowd. Similar decreases in adipsin were not seen in the "cafeteria-fed' rat model, which the authors say is "more representative of simple gluttony.' They add that other experiments indicate there is no problem using the two different species (rat and mouse) in drawing overall conclusions about adipsin.

Based on the recent findings, the authorssuggest that "adipsin meets the initial criteria required of the [adipostat] involved in lipid metabolism or energy balance.' They say the fact that similar enzymes help control blood pressure adds "further credence' to their proposed regulatory role for adipsin. It also may solve the difficult task of determining whether obesity is caused by a metabolic or genetic problem, or by gluttony. If what occurs in rodents holds true in humans, "circulating adipsin levels could serve as a highly useful marker for characterizing obese patients,' conclude the authors.
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Title Annotation:adipsin
Author:Edwards, Diane D.
Publication:Science News
Date:Aug 1, 1987
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