Dietary fats and sodium are both palatable and are hypothesized to synergistically contribute to ingestive behavior and thereby obesity. Contrary to this hypothesis, C57BL/6J mice fed a 45% high fat diet exhibited weight gain that was inhibited by increased dietary sodium content. This suppressive effect of dietary sodium upon weight gain was mediated specifically through a reduction in digestive efficiency, with no effects on food intake behavior, physical activity, or resting metabolism. Replacement of circulating angiotensin II levels reversed the effects of high dietary sodium to suppress digestive efficiency. While the AT1 receptor antagonist losartan had no effect in mice fed low sodium, the AT2 receptor antagonist PD-123,319 suppressed digestive efficiency. Correspondingly, genetic deletion of the AT2 receptor in FVB/NCrl mice resulted in suppressed digestive efficiency even on a standard chow diet. Together these data underscore the importance of digestive efficiency in the pathogenesis of obesity, and implicate dietary sodium, the renin-angiotensin system, and the AT2 receptor in the control of digestive efficiency regardless of mouse strain or macronutrient composition of the diet. These findings highlight the need for greater understanding of nutrient absorption control physiology, and prompt more uniform assessment of digestive efficiency in animal studies of energy balance.

Since the initial description of the granular cell tumor in 1926, numerous other neoplasms, both benign and malignant, have been described to exhibit granular cell change. In most cases, diagnosis remains straightforward via recognition of retained histopathological morphology of the archetypal tumor, despite the presence of focal granular appearance. However, tumors with granular cell differentiation can present a diagnostic challenge either by mimicking alternative diagnoses, or by failing to exhibit architectural clues of the primary entity, thus requiring an immunohistochemical work-up. In light of this, it is important to be aware of the various entities that have been reported to exhibit granular cell morphology. In this review such tumors are discussed along with pertinent clinical and histopathological features.

ObjectivesObstructive sleep apnea (OSA) is a prevalent disease with significant health impacts. While first line therapy is CPAP, long-term compliance is low and device misuse is common, highlighting the need for alternative therapies. Upper airway surgery is one alternative, but substantial side effects hamper efficacy. A new alternative is an implantable hypoglossal nerve stimulator (HNS). These devices utilize neuromodulation to dilate/reinforce the airway and reduce side effects associated with traditional surgery. Several recent trials investigated the efficacy of these devices. The purpose of this study was to perform meta-analysis of available HNS studies investigating treatment of OSA to analyze objective and subjective outcomes and side effects.MethodsA comprehensive literature search of PubMed and Scopus was performed. Two independent reviewers examined clinical trials investigating HNS in treatment of sleep apnea in adults. Studies with objective and subjective endpoints in sleep were included for analysis. Adverse events from trials were also recorded.ResultsAcross 16 studies, 381 patients were analyzed. At 6 months (p = 0.008), mean SAQLI improved by 3.1 (95%CI, 2.6–3.7). At 12 months (p < 0.0001), mean AHI was reduced by 21.1 (95%CI, 16.9–25.3), mean ODI was reduced by 15.0 (95%CI, 12.7–17.4), mean ESS was reduced by 5.0 (95%CI, 4.2–5.8), mean FOSQ improved by 3.1 (95%CI, 2.6–3.4). Pain (6.2%:0.7–16.6), tongue abrasion (11.0%:1.2–28.7), and internal (3.0%:0.3–8.4)/external device (5.8%:0.3–17.4) malfunction were common adverse events.ConclusionsHNS is a safe and effective treatment for CPAP refractory OSA. Further study comparing HNS to other therapies is required.

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