Post-translocation dynamics of black-tailed prairie dogs (Cynomys ludovicianus): A successful conservation and human–wildlife conflict mitigation tool

Prairie dogs have declined by 98% throughout their range in the grasslands of North America. Translocations have been used as a conservation tool to reestablish colonies of this keystone species and to mitigate human–wildlife conflict. Understanding the behavioral responses of prairie dogs to translocation is of utmost importance to enhance the persistence of the species and for species that depend on them, including the critically endangered black-footed ferret. In 2017 and 2018, we translocated 658 black-tailed prairie dogs on the Lower Brule Indian Reservation in central South Dakota, USA, a black-footed ferret recovery site. Here, we describe and evaluate the effectiveness of translocating prairie dogs into augered burrows and soft-released within presumed coteries to reestablish colonies in previously occupied habitat. We released prairie dogs implanted with passive integrated transponders (PIT tags) and conducted recapture events approximately 1-month and 1-year post-release. We hypothesized that these methods would result in a successful translocation and that prairie dogs released as coteries would remain close to where they were released because of their highly social structure. In support of these methods leading to a successful translocation, 69% of marked individuals was captured 1-month post-release, and 39% was captured 1-year post-release. Furthermore, considerable recruitment was observed with 495 unmarked juveniles captured during the 1-year post-release trapping event, and the reestablished colony had more than doubled in the area by 2021. Contrary to our hypothesis, yet to our knowledge a novel finding, there was greater initial movement within the colony 1-month post-release than expected based on recapture locations compared with the published average territory size; however, 1 year after release, most recaptured individuals were captured within the expected territory size when compared to capture locations 1-month post-release. This research demonstrates that while translocating prairie dogs may be socially disruptive initially, it is an important conservation tool.     

Aging modulated by the Drosophila insulin receptor through distinct structure-defined mechanisms

Mutations of the Drosophila melanogaster insulin/IGF signaling system slow aging, while also affecting growth and reproduction. To understand this pleiotropy, we produced an allelic series of single codon substitutions in the Drosophila insulin receptor, InR. We generated InR substitutions using homologous recombination and related each to emerging models of receptor tyrosine kinase structure and function. Three mutations when combined as trans-heterozygotes extended lifespan while retarding growth and fecundity. These genotypes reduced insulin-stimulated Akt phosphorylation, suggesting they impede kinase catalytic domain function. Among these genotypes, longevity was negatively correlated with egg production, consistent with life-history trade-off theory. In contrast, one mutation (InR³⁵³) was located in the kinase insert domain, a poorly characterized element found in all receptor tyrosine kinases. Remarkably, wild-type heterozygotes with InR³⁵³ robustly extended lifespan without affecting growth or reproduction and retained capacity to fully phosphorylate Akt. The Drosophila insulin receptor kinase insert domain contains a previously unrecognized SH2 binding motif. We propose the kinase insert domain interacts with SH2-associated adapter proteins to affect aging through mechanisms that retain insulin sensitivity and are independent of reproduction.     

Ameliorative Effects of Oral Glucosamine on Insulin Resistance and Pancreatic Tissue Damage in Experimental Wistar rats on a High-fat Diet

Hyperlipidemia due to a high-fat diet (HFD) is a risk factor for inducing insulin resistance (IR) and adverse effects on pancreatic β-cells in obesity and type 2 diabetes mellitus. This relationship may be due to activation of the hexosamine-biosynthesis pathway. Administration of exogenous glucosamine (GlcN) can increase the end product of this pathway (uridine-5′-diphosphate-N-acetyl-glucosamine), which can mediate IR and protein glycosylation. The objective of this study was to evaluate the effects of oral GlcN and HFD on IR and pancreatic histologic damage in a 22 wk study of 4 groups of male Wistar rats: control group with normal chow diet, HFD group (24%. g/g lard), GlcN group (500 mg/kg⁻¹ per day of glucosamine hydrochloride in drinking water) and HFD plus oral GlcN. Metabolic variables related to IR that were measured included triglycerides (TG), free fatty acids (FFAs) and malondialdehyde (MDA). Histopathologic evaluation of the pancreas was also performed. The results showed IR in the HFD group, which had increased pancreatic nuclear pyknosis and vacuolization, with fatty infiltration and structural alteration of the islets of Langerhans. TG, FFAs and MDA were higher in serum and pancreatic tissue as compared with the control group. The GlcN group did not develop IR and had only mild nuclear pyknosis with no significant change in the pancreatic content of TG, FFAs and MDA. However, the combined administration of GlcN and HFD attenuated IR and improved TG, FFAs and MDA levels in serum and pancreatic tissue and the pancreatic histopathologic changes, with no significant differences as compared with the control group. These findings suggest that the oral GlcN at a dose of 500 mg/kg⁻¹ is protective against IR and the pancreatic histologic damage caused by HFD.

Obesity, which is an insulin resistance (IR) factor, occurs because of excess caloric intake. Clinically, obesity is associated with high levels of free fatty acids (FFAs) in plasma due to the reduced suppression of lipolysis, is associated with conditions such as diabetes type 2 mellitus, hypertension, atherosclerosis, and metabolic syndrome,² and is an important factor in the pathogenesis of long-term organic damage.³⁶ A previous study⁴⁹ reported that an alteration in the ability of adipocytes to store excess calories as triglycerides (TG) contributes to a greater accumulation of lipids and their metabolites in other tissues. These tissues are not necessarily adapted to their storage, resulting in cellular abnormalities such as apoptosis, oxidative stress, and endoplasmic reticulum stress, which alter cell function. However, both hyperlipidemia and hyperglycemia can have harmful effects on cell function, termed lipotoxicity and glucotoxicity, respectively.^1,36 These effects can lead to desensitization of the target peripheral tissues to the biologic actions of insulin and can also induce an insufficient response of the β cells of the pancreas by glucose stimulation.High-fat diets (HFD) have been associated with hyperlipidemia,³² which in turn leads to IR and pathologic consequences in the pancreas. Hyperlipidemia causes overactivation of the hexosamine biosynthesis pathway (HBP) and overexpression of glutamine:fructose-6-phosphate amidotransferase (GFAT); these give rise to uridine-5′-diphosphate-N-acetyl-glucosamine (UDP-GlcNAc), which causes both IR and alteration of protein glycosylation, leading to selective pancreatic cell destruction.^10,25,44 This pathway can also be activated by administration of exogenous glucosamine (GlcN), suggesting that GlcN in relatively high doses can lead to IR both in vitro and in vivo⁴¹ through an inhibitory effect on early insulin signal transduction,¹⁵ The diabetogenic effect, which is caused in part by interference with glucose utilization in pancreatic cells, reduces insulin release. However, other work²⁰ has argued that exogenous GlcN promotes the development of embryonic pancreatic cells, but did not study pancreatic damage due to subchronic infusion of GlcN in vivo.Although exogenous GlcN is widely used for the treatment of osteoarthritis,^4,40,51 the combination of GlcN with a HFD increases plasma FFAs that can induce IR and affect pancreatic tissue. The objective of the present study was to evaluate the long-term effect of oral GlcN on IR and on pancreatic histopathologic changes produced by a HFD in rats.