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John M. Wilson

Bio: John M. Wilson is an academic researcher from Louisiana State University. The author has contributed to research in topics: Insulin resistance & Prolactin. The author has an hindex of 10, co-authored 16 publications receiving 230 citations.

Papers
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Journal Article•DOI•
TL;DR: The results indicate that the endogenous mechanism controlling seasonality (scotosensitivity and scotorefractoriness) in the Syrian hamster may be reset by drugs that influence serotonergic and catecholaminergic activity.
Abstract: Daily injections of dihydroxyphenylalanine (DOPA), a precursor for dopamine synthesis, given 12 hr after daily injections of 5-hydroxytryptophan (5-HTP), a serotonin precursor, induced uterine growth and increased serum thyroxine and luteinizing hormone (LH) concentrations in scotosensitive female hamsters maintained on short daylengths. On the other hand, daily injections of DOPA given at the same time as daily injections of 5-HTP reduced uterine weights and serum concentrations of thyroxine and LH in scotorefractory female hamsters. These results indicate that the endogenous mechanism controlling seasonality (scotosensitivity and scotorefractoriness) in the Syrian hamster may be reset by drugs that influence serotonergic and catecholaminergic activity. This seasonal mechanism might involve two circadian systems that undergo seasonal changes in their phase relations.

40 citations

Patent•
05 Jun 1996
TL;DR: In this paper, a method for modifying metabolism in a vertebrate animal which entails the administration of pantethine or cysteamine at a predetermined time daily was proposed, which is useful in the treatment of hyperglycemia, glucose intolerance, insulin resistance, and hyperinsulinemia.
Abstract: This invention relates to a method for modifying metabolism in a vertebrate animal which entails the administration of pantethine or cysteamine at a predetermined time daily. The method is useful in the treatment of hyperglycemia, glucose intolerance, insulin resistance, and hyperinsulinemia.

40 citations

Journal Article•DOI•
TL;DR: It is demonstrated that timed daily injections of cortisol and prolactin in specific temporal relationships can produce marked reductions in obesity, hyperinsulinaemia and insulin resistance in the Syrian hamster that persist long after the termination of treatment.
Abstract: Naturally obese female Syrian hamsters were injected daily with prolactin at 0 or 12 h after cortisol injections for 10 days while held in constant light. Controls were similarly injected with saline. Animals were then held on short daylengths (10 h light:14 h darkness) for 10 weeks. They were allowed free access to food and water from birth to time of death. Ten weeks after treatment, retroperitoneal fat stores, plasma concentrations of insulin and glucose, and hypoglycaemic responsiveness to exogenous insulin were determined. The control groups as well as the 12-h hormone treatment group were obese, hyperinsulinaemic and insulin resistant. However, the 0-h treatment dramatically reduced retroperitoneal fat stores (41-55%), plasma insulin concentration (60-70%) and the insulin to glucose ratio (63-68%) compared with controls. Values for these parameters in the 0-h treatment groups were similar to those of their lean litter-mates. Furthermore, the 0-h group but not the 12-h group was more sensitive than control animals to the hypoglycaemic effects of exogenous insulin at doses 0.2 and 2.0 U/kg body weight. These results demonstrate that timed daily injections of cortisol and prolactin in specific temporal relationships can produce marked reductions in obesity, hyperinsulinaemia and insulin resistance in the Syrian hamster that persist long after the termination of treatment. This study also suggests an important role for the interactions of circadian neuroendocrine systems in the regulation of these metabolic states.

29 citations

Patent•
20 Jun 1995
TL;DR: In this article, methods for improving various aberrant metabolic indices in mammals including humans by administration of muscarinic (particularly M1) receptor antagonists alone or in combination with prolactin inhibiting compounds.
Abstract: Disclosed are methods for improving various aberrant metabolic indices in mammals including humans by administration of muscarinic (particularly M1) receptor antagonists alone or in combination with prolactin inhibiting compounds. Preferably the administration takes place at a predetermined time (or, if a combination of muscarinic receptor antagonist and prolactin inhibitor is used, at different predetermined times) during a 24-hour period when the administration is effective (or its effect more pronounced). The invention has application in the treatment of lipid and glucose metabolism disorders.

23 citations

Patent•
05 Jun 1996
TL;DR: In this article, methods for regulating or ameliorating lipid and glucose metabolism and reducing in a vertebrate animal body fat stores, insulin resistance, hyperinsulinemia, hyperglycemia, hyperlipidemia, elevated blood lipoproteins (such as triglycerides and cholesterol including chylomicrons, VLDL and LDL) and/or increasing in the subject the plasma HDL.
Abstract: Disclosed herein are methods for regulating or ameliorating lipid and glucose metabolism and reducing in a vertebrate animal body fat stores, insulin resistance, hyperinsulinemia, hyperglycemia, hyperlipidemia, elevated blood lipoproteins (such as triglycerides and cholesterol including chylomicrons, VLDL and LDL) and/or increasing in the subject the plasma HDL. The methods comprise administration or timed administration of inhibitors or dopamine beta hydroxylase (DBH).

19 citations


Cited by
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Journal Article•DOI•
TL;DR: Both dopamine D1/D5 receptor agonists, which are positively coupled to adenylyl cyclase, and a cAMP phosphodiesterase inhibitor ameliorated the physiological as well as the memory defects, consistent with the idea that the cAMP-protein kinase A-dependent signaling pathway is defective in age-related spatial memory loss.
Abstract: To study the physiological and molecular mechanisms of age-related memory loss, we assessed spatial memory in C57BL/B6 mice from different age cohorts and then measured in vitro the late phase of hippocampal long-term potentiation (L-LTP). Most young mice acquired the spatial task, whereas only a minority of aged mice did. Aged mice not only made significantly more errors but also exhibited greater individual differences. Slices from the hippocampus of aged mice exhibited significantly reduced L-LTP, and this was significantly and negatively correlated with errors in memory. Because L-LTP depends on cAMP activation, we examined whether drugs that enhanced cAMP would attenuate the L-LTP and memory defects. Both dopamine D1/D5 receptor agonists, which are positively coupled to adenylyl cyclase, and a cAMP phosphodiesterase inhibitor ameliorated the physiological as well as the memory defects, consistent with the idea that a cAMP–protein kinase A-dependent signaling pathway is defective in age-related spatial memory loss.

565 citations

01 Jan 2000
TL;DR: In this article, the authors reviewed the current understanding of T cell immunobiology and the critical role of inflammatory processes during pregnancy and discussed lessons derived from studies on the regulation of t cell responsiveness during mammalian gestation are considered in the wider context of T-cell tolerance toward some microbial infections and tumors, avoidance of auto-unity, and tissue allograft rejection.
Abstract: Mammalian reproduction poses an immunological paradox because fetal alloantigens encoded by genes inherited from the father should provoke responses by maternal T cells leading to fetal loss. Current understanding of T cell immunobiology and the critical role of inflammatory processes during pregnancy is reviewed and discussed. Lessons derived from studies on the regulation of T cell responsiveness during mammalian gestation are considered in the wider context of T cell tolerance toward some microbial infections and tumors, avoidance of autoim- munity, and tissue allograft rejection.

274 citations

Journal Article•DOI•
TL;DR: In this paper, the authors reviewed the current understanding of T cell immunobiology and the critical role of inflammatory processes during pregnancy and discussed lessons derived from studies on the regulation of t cell responsiveness during mammalian gestation are considered in the wider context of T-cell tolerance toward some microbial infections and tumors, avoidance of autoimmunity, and tissue allograft rejection.
Abstract: Mammalian reproduction poses an immunological paradox because fetal alloantigens encoded by genes inherited from the father should provoke responses by maternal T cells leading to fetal loss. Current understanding of T cell immunobiology and the critical role of inflammatory processes during pregnancy is reviewed and discussed. Lessons derived from studies on the regulation of T cell responsiveness during mammalian gestation are considered in the wider context of T cell tolerance toward some microbial infections and tumors, avoidance of autoimmunity, and tissue allograft rejection.

273 citations

Patent•
02 Feb 1999
TL;DR: In this article, the authors present methods and compositions for modification and regulation of glucose and lipid metabolism, generally to reduce insulin resistance, hyperglycemia, hyperinsulinemia, obesity, hyperlipidemia, hyper-lipoproteinemia (such as chylomicrons, VLDL and LDL), and to regulate body fat and more generally lipid stores, and, more generally, for the improvement of metabolism disorders, especially those associated with diabetes, obesity and/or atherosclerosis.
Abstract: The present invention provides methods and compositions for modification and regulation of glucose and lipid metabolism, generally to reduce insulin resistance, hyperglycemia, hyperinsulinemia, obesity, hyperlipidemia, hyperlipoprotein-emia (such as chylomicrons, VLDL and LDL), and to regulate body fat and more generally lipid stores, and, more generally, for the improvement of metabolism disorders, especially those associated with diabetes, obesity and/or atherosclerosis.

222 citations

Journal Article•DOI•
TL;DR: This work provides evidence pointing toward the sympathetic nervous system as a likely mediator of the effects of MEL on short day-induced body fat decreases in Siberian hamsters through increases in sympathetic drive on WAT and BAT.
Abstract: It appears advantageous for many non-human animals to store energy body fat extensively and efficiently because their food supply is more labile and less abundant than in their human counterparts. The level of adiposity in many of these species often shows predictable increases and decreases with changes in the season. These cyclic changes in seasonal adiposity in some species are triggered by changes in the photoperiod that are faithfully transduced into a biochemical signal through the nightly secretion of melatonin (MEL) via the pineal gland. Here, we focus primarily on the findings from the most commonly studied species showing seasonal changes in adiposity-Siberian and Syrian hamsters. The data to date are not compelling for a direct effect of MEL on white adipose tissue (WAT) and brown adipose tissue (BAT) despite some recent data to the contrary. Thus far, none of the possible hormonal intermediaries for the effects of MEL on seasonal adiposity appear likely as a mechanism by which MEL affects the photoperiodic control of body fat levels indirectly. We also provide evidence pointing toward the sympathetic nervous system as a likely mediator of the effects of MEL on short day-induced body fat decreases in Siberian hamsters through increases in sympathetic drive on WAT and BAT. We speculate that decreases in the SNS drive to these tissues may underlie the photoperiod-induced seasonal increases in body fat of species such as Syrian hamsters. Clearly, we need to deepen our understanding of seasonal adiposity, although, to our knowledge, this is the only form of environmentally induced changes in body fat where the key elements of its external trigger have been identified and can be traced to and through their transduction into a physiological stimulus that ultimately affects identified responses of white adipocyte physiology and cellularity. Finally, the comparative physiological approach to the study of seasonal adiposity seems likely to continue to yield significant insights into the mechanisms underlying this phenomenon and for understanding obesity and its reversal in general.

217 citations