The effects of crowding stress on the pancreatic islets morphology in golden hamsters.

Behavior and the pancreatic islets morphology of golden hamsters exposed for different periods (24 h, 15 and 30 d) to crowding stress were investigated. The crowding induced an intensive turmoil and enhanced irritability and aggressiveness, particularly among the female specimens. Within a week, a rank hierarchy seemed to establish and therefore, later the fighting incidence was more reduced. Marked morphological alterations were recorded in the endocrine pancreas, affecting in various degrees all cell types, but especially the insulin-producing cells. The B-cells showed increased sizes, higher incidence of mitotic divisions, a drastical reduction of secretory granules amounts, enlargement of GOLGI complexes, mitochondria swelling and extension of the ergastoplasm. On the other hand, after 30 d, part of these cells displayed pycnotic nuclei, large cytoplasmic vacuoles and increased number of lasosomes and lipid inclusions. Due to the B-cell hyperplasia, the relative number of both A1- and A2-cells per islet occurred diminished and their typical localization modified. The islets of 15 and 30 d crowded specimens showed enlarged sinusoids and clear peri-insular spaces. The above morphological modifications, which suggest as a whole the global stimulation of gland secretory activity, are presented in relation with other authors findings. The presumably involvements of adrenal-cortex and -medulla hormones in the mediation of stress-induced glycemic and pancreatic alterations are discussed.     

Phospholipid methylation in pancreatic islets

Glucose provokes a transient stimulation of phospholipid methylation in rat pancreatic islets, possibly by increasing phospholipid methyltransferase activity. The association of DL-homocysteine and 3-deazaadenosine inhibits phospholipid methylation. The methylation of phospholipids may play a role in the stimulus-secretion coupling for glucose-induced insulin release.     

Transglutaminase activity in pancreatic islets

1. Pancreatic islet homogenates catalyze, in a Ca²⁺-dependent fashion, the incorporation of [2,5-³H]histamine, [1,4-¹⁴C]putrescine, [1,2-³H]agmatine, [¹⁴C]methylamine, L-[U-¹⁴C]lysine in N,N-dimethylcasein. 2. Using [2,5-³H]histamine as the amine donor, the K_m for Ca²⁺ and histamine amounts to 90μM and 0.7 mM, respectively. 3. The incorporation of [2,5-³H]histamine into N,N-dimethylcasein is inhibited by monodansylcadaverine, N-p-tosyl glycine, bacitracin and methylamine, the relative extent of inhibition depending on the respective concentrations of Ca²⁺, inhibitor and amine donor. 4. Bacitracin and methylamine, but not N-p-tosyl glycine, cause a dose-related inhibition of glucose-stimulated insulin release. 5. It is concluded that, in pancreatic islets, the Ca²⁺-responsive transglutaminase activity plays a critical role in the process of glucose-induced insulin release.     

Presence of fructokinase in pancreatic islets

Homogenates of rat pancreatic islets that had been heated for 5 min at 70 degrees C to inactive hexokinases, catalyzed the ATP-dependent phosphorylation of D-fructose. This reaction was dependent on the presence of K+ and was inhibited by D-tagatose although not by D-glucose or D-glucose 6-phosphate. The phosphorylation product was identified as fructose 1-phosphate through its conversion to a bisphosphate ester by Clostridium difficile fructose 1-phosphate kinase. These findings allowed the conclusion that fructokinase (ketohexokinase) was responsible for this process. Similar results were observed with tumoral insulin-producing cells (RINm5F line). Fructokinase may account for a large share of fructose phosphorylation in intact islets, particularly in the presence of D-glucose.     

Asynchrony in the estrous cycles of golden hamsters (Mesocricetus auratus)

The golden hamster has been described as exhibiting estrous cycle synchrony caused by social dominance. This has recently been reexamined by J. C. Schank (2000, Horm. Behav. 38, 94-101) with the aid of computer simulations. He concluded that there is no evidence for cycle synchrony among golden hamsters. In the present article we confirm this theoretical approach with the help of long-term experiments. Indeed, estrous cycle asynchrony was observed. Singly housed female golden hamsters in phase with their neighbors and in physical contact desynchronized their 4-day cycles after 2 or 3 weeks. Asynchrony was caused mainly by stochastic 5-day cycles. Statistical analysis was performed using a Monte-Carlo bootstrap approach. Based on the empirical data, an individual-based computer model was developed to simulate the dynamics of cycle desynchronization. Potential advantages were deduced for the population level. It emerged that estrous cycle asynchrony led to higher reproductive success for females where the probability of fertilization was low (e.g., after hibernation, poor habitat).     

Predictors of dominance in the male golden hamster (Mesocricetus auratus)

The outcome of social interactions between four male hamsters was significantly related to body weight (r_s=0·66) and to the size and pigmentation of their lateral flank glands (r_s=0·82). Weight was held constant in a second experiment and variations in gland size and pigmentation remained significantly related to the outcome of social encounters (r_s=0·77). In a third experiment, castrate hamsters of uniform weight receiving either no hormone, 0·1 mg, 0·50 mg, or 1·00 mg testosterone propionate exhibited flank gland variations significantly related to social rank (r_s=0·81). These experiments demonstrate that the state of the flank gland, which is related to endogenous androgen levels, can be used as a predictor of social rank in male hamsters.     

Protein profiling of pancreatic islets

The insulin-producing β cell in the islet of Langerhans is central in glucose homeostasis. Its dysfunction is part of the pathogenesis of both Type 1 and 2 diabetes mellitus. In both forms of the disease, there is a cytotoxic component either induced by cytokines, as in Type 1 diabetes, or by elevated levels of glucose and fatty acids, as in Type 2 diabetes. To find the mechanisms responsible for the cytotoxic effects of these compounds proteomic approaches with 2D gel electrophoresis and surface-enhanced laser desorption/ionization time-of-flight mass spectrometry have been undertaken. In this article, we describe these methods, and other methodological aspects of protein profiling of pancreatic islets, and summarize the results obtained with these methods.     

Electroencephalography in the diagnosis of hydrocephalus in golden hamsters (Mesocricetus auratus)

The golden hamster (Mesocricetus auratus) is a popular laboratory animal and is used in a multitude of behavioural studies. However, it has been shown that it suffers from different forms of hereditary hydrocephalus, which may result in behavioural changes. This prospective study was designed to look into the usefulness of electroencephalography (EEG) measurements in the diagnosis of hydrocephalus in hamsters. The EEGs of the hydrocephalic hamsters were evaluated double-blind and showed a high-voltage slow wave activity, with a fast activity superimposed onto it. This pattern has already been well described in other hydrocephalic species and differed significantly from the EEGs that were obtained from the normal hamsters. It was concluded from our study that a background activity with an amplitude over 50 muV in combination with a frequency of < or =5 Hz was highly indicative of hydrocephalus in young hamsters. We believe that the EEG could be a very useful diagnostic tool in the screening for hydrocephalus in hamsters.     

Protein profiling of pancreatic islets

The insulin-producing beta cell in the islet of Langerhans is central in glucose homeostasis. Its dysfunction is part of the pathogenesis of both Type 1 and 2 diabetes mellitus. In both forms of the disease, there is a cytotoxic component either induced by cytokines, as in Type 1 diabetes, or by elevated levels of glucose and fatty acids, as in Type 2 diabetes. To find the mechanisms responsible for the cytotoxic effects of these compounds proteomic approaches with 2D gel electrophoresis and surface-enhanced laser desorption/ionization time-of-flight mass spectrometry have been undertaken. In this article, we describe these methods, and other methodological aspects of protein profiling of pancreatic islets, and summarize the results obtained with these methods.     

Histochemistry of Langerhans' islets in the pancreas of cattle (Bos Taurus L.)

Summary A and B cells in the pancreatic islets of cattle are interlaced with one another. The histochemical characteristics of the islet cells is similar to that of some other mammals. Series of differences are however detected concerning: the positive reaction for glucose-6-phosphatase in the A cells and in the epithelium of the excretory ducts, the simultaneous presence of alkaline phosphatase in the A and B cells, a higher contents of phospholipids in the B cells and a lack of histochemically provable zinc. These differences in the histochemistry of the pancreatic islets of cattle are in authors, opinion an expression of peculiarity of the species.     

Ionophoretic activity in pancreatic islets.

Extracts of pancreatic islets stimulate the translocation of calcium from an aqueous into an organic immiscible phase. This ionophoretic activity, which is derived mainly from membrane-rich subcellular fractions, displays several features in common with that of A23187 in the same model. The phenomenon of calcium translocation caused by either the islet extract or the antibiotic ionophore represents a power function of the concentration of ionophoretic material; it is saturable at high calcium concentrations, affected by the concentration of Na⁺ and pH of the aqueous phase, increased at low temperature, and inhibited by suloctidil, the latter inhibitory effect being antagonized by calcium itself. These findings underline the potential significance of native ionophores in the regulation of calcium movements across membrane systems in the islet cells.     

Resistin is expressed in pancreatic islets

Resistin, a recently described adipocyte factor, is regulated by peroxisome proliferator-activated receptor gamma (PPARgamma) agonists. While resistin has been proposed to mediate insulin resistance in rodents, little is known about human resistin and its expression in pancreatic islets has not been tested. The goal of the present study was therefore to analyze whether resistin, like PPARgamma, is expressed in islets. Human islets from seven donors were analyzed by quantitative RT-PCR revealing resistin expression in all samples. Immunohistochemistry using a resistin-specific antibody on human pancreatic sections localized resistin protein to the islets. Mouse resistin was also detected in the Min6 beta cell line. Interestingly, we found a 4-fold increase in islet resistin expression in insulin resistant A-ZIP transgenic compared to wild-type mice. Our results demonstrate that resistin is expressed in islets and up-regulated in insulin resistance and thereby shed new light on the role of resistin in mice and humans.