Colorful ornaments have been the focus of sexual selection studies since the work of Darwin. Yellow to red coloration is often produced by carotenoid pigments. Different hypotheses have been formulated to explain the evolution of these traits as signals of individual quality. Many of these hypotheses involve the existence of a signal production cost. The carotenoids necessary for signaling can only be obtained from food. In this line, carotenoid-based signals could reveal an individual's capacity to find sufficient dietary pigments. However, the ingested carotenoids are often yellow and became transformed by the organism to produce pigments of more intense color (red ketocarotenoids). Biotransformation often involves oxidation reactions. We tested the hypothesis that biotransformation could be costly because a certain level of oxidative stress is required. Thus, the carotenoid-based signals could reveal the efficiency of the owner in successfully managing this challenge. In a bird with ketocarotenoid-based ornaments (the red-legged partridge; Alectoris rufa), the availability of different carotenoids in the diet and oxidative stress were manipulated. We found that color and pigment levels in the ornaments depended on the relative quantity in the food of those carotenoids used as substrates in biotransformation (i.e. zeaxanthin and lutein). Moreover, we found that birds exposed to certain levels of a free radical generator (diquat) developed redder bills and deposited higher amounts of ketocarotenoids (astaxanthin) in ornaments, thus supporting the hypothesis. However, the effect also depended on the relative abundance of substrate carotenoids in the diet. This last result suggests the involvement of a resource allocation trade-off, which would support, to some extent, a signaling cost linked to carotenoid acquisition. PeerJ Preprints | https://doi.org/10.7287/peerj.preprints.1873v1 | CC-BY 4.0 Open Access | rec Abstract 1 Colorful ornaments have been the focus of sexual selection studies since the work of 2 Darwin. Yellow to red coloration is often produced by carotenoid pigments. Different 3 hypotheses have been formulated to explain the evolution of these traits as signals of 4 individual quality. Many of these hypotheses involve the existence of a signal production 5 cost. The carotenoids necessary for signaling can only be obtained from food. In this line, 6 carotenoid-based signals could reveal an individual's capacity to find sufficient dietary 7 pigments. However, the ingested carotenoids are often yellow and became transformed by 8 the organism to produce pigments of more intense color (red ketocarotenoids). 9 Biotransformation often involves oxidation reactions. We tested the hypothesis that 10 biotransformation could be costly because a certain level of oxidative stress is required. 11 Thus, the carotenoid-based signals could reveal the efficiency of the owner in successfully 12 managing this challenge. In a bird with ketocarotenoid-based ornaments (the red-legged 13 partridge; Alectoris rufa), the ava...

In both type 1 and type 2 diabetes, diabetic complications in target organs arise from chronic elevations of glucose. The pathogenic effect of high glucose, possibly in concert with fatty acids, is mediated to a significant extent via increased production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) and subsequent oxidative stress. ROS and RNS directly oxidize and damage DNA, proteins, and lipids. In addition to their ability to directly inflict damage on macromolecules, ROS and RNS indirectly induce damage to tissues by activating a number of cellular stress-sensitive pathways. These pathways include nuclear factor-B, p38 mitogen-activated protein kinase, NH 2 -terminal Jun kinases/stress-activated protein kinases, hexosamines, and others. In addition, there is evidence that in type 2 diabetes, the activation of these same pathways by elevations in glucose and free fatty acid (FFA) levels leads to both insulin resistance and impaired insulin secretion. Therefore, we propose here that the hyperglycemia-induced, and possibly FFA-induced, activation of stress pathways plays a key role in the development of not only the late complications in type 1 and type 2 diabetes, but also the insulin resistance and impaired insulin secretion seen in type 2 diabetes. Diabetes

The effects of a vitamin D deficiency on insulin and glucagon release was determined in the isolated perfused rat pancreas by radioimmunoassay of the secreted proteins. During a 30-minute period of perfusion with glucose and arginine, pancreases from vitamin D-deficient rats exhibited a 48 percent reduction in insulin secretion compared to that for pancreases from vitamin D-deficient rats that had been replenished with vitamin D. Vitamin D status had no effect on pancreatic glucagon secretion. This result, along with the previously demonstrated presence in the pancreas of a vitamin D-dependent calcium-binding protein and cytosol receptor for the hormonal form of vitamin D, 1,25-dihydroxyvitamin D3, indicates an important role for vitamin D in the endocrine functioning of the pancreas.

A B S T R ACT Phases of insulin release were studied in the perfused pancreas during a variety of glucose stimulation patterns. Patterns included staircase stimulations, constant prolonged single steps, restimulations, and ramp functions. Except at low concentrations, prolonged single steps of glucose elicited early spikes of insulin and a slowly rising second phase. Total insulin in the initial spikes increased with higher glucose concentrations. However, the time-related pattern of these spikes was similar in all cases; ratios of initial secretion rate to total insulin released were constant. Total insulin released in this early phase approximated a sigmoidal function of glucose concentration; mathematical differentiation of this function gave a skewed bell-shaped distribution curve. Staircase stimulations caused insulin to be released as a series of transient spikes which did not correlate with the increment of glucose but rather to the available insulin for a given glucose concentration minus that released in previous steps. The sum of total insulin released as spikes in a staircase series leading to a given glucose concentration was the same as when that concentration was used as a single step. Interrupted prolonged glucose infusions indicated the second phase of insulin release could prime the pancreas and that the first and second phases were interrelated. When glucose was perfused as ramp functions of slow, increasing, concentration, phasic response disappeared.A previous two-compartmental model was expanded to include a threshold or sensitivity distribution hypothesis. This hypothesis proposes that labile insulin is not stored in a homogeneous form but as packets with a bell-shaped distribution of thresholds to glucose. These packets respond quickly when their threshold levels to

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Abstract. To determine if glucagon secretion is under physiological control of intra-islet insulin, pancreata from normal rats were perfused at a 100 mg/dl glucose concentration with either guinea pig antiinsulin serum or normal guinea pig serum in a nonrecirculating system. Perfusion of antiserum was followed within 3 min by a significant rise in glucagon that reached peak levels three times the base-line values and assumed a hectic pattern that returned rapidly to base-line levels upon termination of the antiserum perfusion. Nonimmune guinea pig serum had no effect.To gain insight into the probable site of insulin neutralization, '25I-labeled human 'y-globulin was added to antiserum or nonimmune serum and perfused for 3 min. More than 83% of the radioactivity was recovered in the effluent within 3 min after termination of the infusion, and only 0.05±0.015% of the radioactivity injected was present in the pancreas 10 min after the perfusion. The

The effect of carbohydrates on the secretion of immunochemically measurable insulin was studied in an isolated perfused pancreatic preparation from the rat. Degradation of circulating insulin (as measured by chromatographic examination of added insulin-I131) was less than 15% during the 4-hr experimental period. Without the addition of glucose, or at glucose concentrations of less than 50 mg/100 ml, insulin secretion was not detectable. At glucose concentrations of 50–150 mg/100 ml, insulin secretion occurred immediately and persisted throughout the experimental period. Insulin secretion was further increased by increasing glucose concentration to 150–500 mg/100 ml. The incidence of islet cell degranulation increased with increasing insulin secretion, suggesting that glucose stimulated secretion of stored insulin faster than synthesis of insulin de novo. Galactose, xylose, l-arabinose, pyruvate, and 2-deoxyglucose in concentrations of 600 mg/100 ml did not stimulate insulin secretion. Mannose stimulated the pancreas equally as well as glucose. Fructose was also active, but was less effective than glucose. Neither 2-deoxyglucose nor galactose blocked the insulin secretion by glucose. The data suggest that secretion of insulin is stimulated by a metabolite or a product resulting from the metabolism of glucose which can also be supplied by other metabolizable sugars.

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