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Mowbray, S.

Publications and source records attributed to Mowbray, S..

2 recordsLinked to original sources

Back to the Meadow Brown: eyespot variation and field temperature in a classic butterfly polymorphism

Since the classic work of E.B. Ford, alternate hypotheses have focused on explaining eyespot variation in the Meadow Brown butterfly strictly as a genetic polymorphism and the role of temperature in this classic example of natural selection has therefore been overlooked. Here we use large and continuous field collections from three sites in the UK to examine the effect of field temperature on total eyespot variation using the same presence/absence scoring as Ford. We show that higher developmental temperatures in the field lead to the disappearance of the spots visible while the butterfly is at rest, explaining Fords original observation that hindwing spotting declines across the season as temperatures increase. Analysis of wing damage supports the historical hypothesis that hindwing spots confuse aerial predators. However, as hindwing spotting declines over the season, a trade-off is suggested between their role in deflecting predators early in the season and their later developmental cost. In contrast, the large forewing eyespot is always present, scales with forewing length and its variation is best explained by day of the year rather than developmental temperature. As this large forewing spot is thought to be involved in startling predators, its constant presence is therefore likely required for defence. We model annual total spot variation with phenological data from the UK and derive predictions as to how spot patterns will continue to change under increasing summer temperatures, predicting that spotting will continue to decrease both across a single season and year or year as our climate warms. Summary statementWe show that a long-held example of genetic polymorphism, eyespot variation is the Meadow Brown butterfly, is correlated with field temperature during butterfly development.

ecology↗

FGF21 Normalizes Plasma Glucose in Mouse Models of Type 1 Diabetes and Insulin Receptor Dysfunction

Fibroblast growth factor 21 (FGF21) is a member of the fibroblast growth factor (FGF) family of proteins. The biological activity of FGF21 was first shown to induce insulin independent glucose uptake in adipocytes through the GLUT1 transporter. Subsequently, it was shown to have effects on the liver to increase fatty acid oxidation. FGF21 treatment provides beneficial metabolic effects in both animal models and patients with obesity, type 2 diabetes mellitus (T2D) and/or fatty liver disease. In this paper, we revisited the original finding and found that insulin independent glucose uptake in adipocytes is preserved in the presence of an insulin receptor antagonist. Using a 40 kDa PEGylated (PEG) and half-life extended form of FGF21 (FGF21-PEG), we extended these in vitro results to two different mouse models of diabetes. FGF21-PEG normalized plasma glucose in streptozotocin-treated mice, a model of type 1 diabetes (T1D), without restoring pancreatic {beta}-cell function. FGF21-PEG also normalized plasma glucose levels and improved glucose tolerance in mice chronically treated with an insulin competitive insulin receptor antagonist, a model of autoimmune/Type-B insulin resistance. These data extend the pharmacological potential of FGF21 beyond the settings of T2D, fatty liver and obesity.

pharmacology and toxicology↗