Am J Physiol Endocrinol Metab
Department of Pharmacology and Toxicology, School of Medicine Dayton, Wright State University, Ohio, United States.
Published: November 2023
Male mice lacking the Na-K-2Cl cotransporter () specifically in insulin-secreting β-cells () have reduced β-cell mass and mild β-cell secretory dysfunction associated with overweight, glucose intolerance, insulin resistance, and metabolic abnormalities. Here, we confirmed and extended previous results to female mice, which developed a similar metabolic syndrome-like phenotype as males, albeit milder. Notably, male and female mice developed overweight without consuming excess calories. Analysis of the feeding microstructure revealed that young lean male mice ate meals of higher caloric content and at a relatively lower frequency than normal mice, particularly during the night. In addition, overweight mice consumed significantly larger meals than lean mice. Therefore, the reduced satiation control of feeding precedes the onset of overweight and is worsened in older mice. However, the time spent between meals remained intact in lean and overweight mice, indicating conserved satiety responses to ad libitum feeding. Nevertheless, satiety was intensified during and after refeeding only in overweight males. In lean females, satiety responses to refeeding were delayed relative to age- and body weight-matched control mice but normalized in overweight mice. Since meal size did not change during refeeding, these data suggested that the satiety control of eating after fasting is impaired in lean mice before the onset of overweight and independently of their reduced satiation responses. Therefore, our results support the novel hypothesis that reduced satiation precedes the onset of overweight and the development of metabolic dysregulation. Obesity, defined as excess fat accumulation, increases the absolute risk for metabolic diseases. Although obesity is usually attributed to increased food intake, we demonstrate that body weight gain can be hastened without consuming excess calories. In fact, impaired meal termination control, i.e., satiation, is detectable before the development of overweight in an animal model that develops a metabolic syndrome-like phenotype.
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http://dx.doi.org/10.1152/ajpendo.00197.2023 | DOI Listing |
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