Defining comparative physiology: results from an online survey and systematic review.

August Krogh's 1929 principle is referenced as the cornerstone of comparative physiology (CP). However, there are diverse views as to what type of research falls under the CP approach. This study had three aims: 1) determine how CP is defined through an online survey (OS) of physiologists and a systematic review (SR), 2) put forth an updated definition of CP by summarizing OS and SR results, and 3) outline the numerous CP research approaches. Professional physiology societies (n = 54) were invited to share the OS with their members, and a SR was conducted, which yielded 197 and 70 definitions, respectively. The three most common words in descending order in the OS definitions were "different," "animals," and "species" and in the SR definitions, "animals," "species," and "organisms." The three most prevalent themes from the OS and SR definitions were comparing/differences/diversity across species (78% and 51%, respectively), response to the environment/ecology (28% and 43%, respectively), and included evolution or adaptation (24% and 60%, respectively). Ten research approaches were identified, which include broad comparison (i.e., many species generalization), specific comparison (e.g., 2 species; for traits that are different, exaggerated, extreme, missing, or not induced), or comparison while considering evolution (i.e., evolutionary physiology), ecology (i.e., ecophysiology), or human physiology/medicine. Only 5% and 33% of OS and SR definitions described or mentioned Krogh's principle. In conclusion, CP can best be defined as a compilation of research approaches that utilize different types of comparisons to elucidate physiological mechanisms and not simply comparing physiologies as the name implies.

Novel Organic Mineral Complex Prevents High-Fat Diet-Induced Changes in the Gut and Liver of Male Sprague-Dawley Rats.

Diet-induced obesity and metabolic syndrome are associated with the onset of gastrointestinal diseases, such as hepatic steatosis and gut inflammation. Prior research shows that a proprietary soil-derived organic mineral complex (OMC) prevents hyperglycemia, endotoxemia, and liver injury in rats fed a high-fat diet (HFD) for 10 weeks. The aim of this study was to further examine the effects of OMC on the liver and gastrointestinal health of these rats. Six-week-old male Sprague-Dawley rats (n = 36) were divided into two dietary groups: Chow or HFD fed for 10 weeks. Animals were further divided (n = 6/group) and administered 0, 0.6, or 3.0 mg/mL OMC in their drinking water. The 10-week HFD resulted in significant liver fat accumulation. Both OMC doses prevented hepatic increases in the glycation end product Nε-(carboxymethyl)lysine (CML) induced by HFD (p < 0.05). Low-dose OMC was associated with higher expression of occludin in the small intestine of rats fed either diet (two-way ANOVA, p < 0.042). Linear discriminant analysis (LDA) effect size (LEfSe) indicated significant differences in fecal microbial composition of untreated HFD-fed rats in comparison to untreated Chow rats at 10 weeks (LDA score > 2.0 : 18). After 10 weeks, untreated HFD-fed rats were also more abundant in bacteria associated with obesity and metabolic disease in comparison to corresponding week 0 samples (LDA score > 2.0 : 31), 10-week untreated Chow (LDA > 2.0 : 18), or 10-week OMC-treated HFD-fed rats (0.6 mg/mL; LDA > 2.0 : 80, 3.0 mg/mL; LDA > 2.0 : 8). Low-dose OMC prevented the HFD-induced increase in the Firmicutes-to-Bacteroidetes (F/B) ratio (p < 0.0416). Study animals treated with OMC exhibited no significant changes in the gut microbiota at week 10, although gut inflammatory biomarkers were not significantly altered by diet or OMC treatment. These results indicate that OMC supplementation ameliorates glycosylation reactions and modifies HFD-induced alterations in the intestinal microbiota.

High fat feeding impairs endothelin-1 mediated vasoconstriction through increased iNOS-derived nitric oxide.

Rats fed a high fat diet develop increased adiposity and oxidative stress leading to impaired vasodilation. The purpose of the present study was to examine the effects of high fat-induced increases in adiposity and oxidative stress on vasoconstrictor reactivity of isolated mesenteric arteries. We hypothesized that rats with more adiposity would develop oxidative stress-potentiated increases in iNOS-derived nitric oxide leading to diminished vasoconstriction. Male Sprague-Dawley rats were fed either a control (Chow) or high fat diet for 6 weeks. The roles of oxidative stress and iNOS in the impaired vasoconstrictor responses to endothelin-1 were characterized in small mesenteric arteries. Rats fed the HFD developed significantly more adiposity compared to Chow rats. Plasma levels of nitric oxide and the inflammatory factor tumor necrosis factor α were significantly higher in high fat fed rats compared to Chow rats (nitric oxide: 95.36±19.3 vs. 38.96±6.7 µM; tumor necrosis factor α: 598±111.4 vs. 292±71.8 pg/ml, respectively). Despite exhibiting elevated systolic blood pressure compared to Chow rats (153.5±2.4 vs. 137.5±2.7 mm Hg), endothelin-1 mediated vasoconstriction was impaired in isolated mesenteric arteries from high fat fed rats but was normalized by individual or combined inhibition of nitric oxide synthase, iNOS, or oxidative stress. Therefore, oxidative stress and iNOS are involved in the attenuation of endothelin-1 mediated vasoconstriction observed in isolated mesenteric arteries from high fat fed rats.