Unique alterations of neuropeptide content in median eminence, amygdala, and dorsal vagal complex of 3- and 6-week-old diabetes mutant mice

Timmers, Kim I.; Palkovits, Miklós; Coleman, D L

doi:10.1016/0026-0495(90)90088-t

Cited by 10 publications

(2 citation statements)

References 45 publications

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“…Blood glucose levels in the diabetic females were greater than in the male diabetics. Circulating insulin levels, although not measured in this study, have been shown to be comparable in male and female db/db mice at 3 weeks of age (Timers et al, 1990) and slightly greater in male versus female at 8 weeks of age (E.M. Gibbs, personal communication). Both male gender and diabetes significantly increased mortality, P < 0.05 for each; however, there was no significant interaction of gender and diabetes on mortality.…”

Section: Resultsmentioning

confidence: 51%

Experimental Stroke in the Female Diabetic, db/db, Mouse

Vannucci

Willing

Goto

et al. 2001

J Cereb Blood Flow Metab

139

135

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Diabetic hyperglycemia increases brain damage after cerebral ischemia in animals and humans, although the underlying mechanisms remain unclear. Gender-linked differences in ischemic tolerance have been described but have not been studied in the context of diabetes. In the current study, we used a model of unilateral common carotid artery ligation, combined with systemic hypoxia, to study the effects of diabetes and gender on hypoxic-ischemic (HI) brain damage in the genetic model of Type II diabetes, the db/db, mouse. Male and female, control and db/db, mice were subjected to right common carotid artery ligation followed by varying periods of hypoxia (8% oxygen/92% nitrogen) to assess mortality, infarct volume, and tissue damage by light microscopic techniques. End-ischemic regional cerebral blood flow (CBF) was determined using [14C] iodoantipyrine autoradiography. Glycolytic and high energy phosphate compounds were measured in blood and brain by enzymatic and fluorometric techniques. Gender and diabetes had significant effects on mortality from HI and extent of brain damage in the survivors. Female mice were more resistant than their male counterparts, such that the severity (mortality and infarction size) in the male diabetics > female diabetics - male controls > female controls. Endischemic CBF and depletion of cerebral high energy reserves were comparable among all groups. Surprisingly, female diabetic mice were more hyperglycemic and demonstrated a greater prolonged lactacidosis than the males; however, they were more resistant to damage. The results suggest a unique pathophysiology of hypoxia-ischemia in the female diabetic brain.

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Section: Resultsmentioning

confidence: 51%

Experimental Stroke in the Female Diabetic, db/db, Mouse

Vannucci

Willing

Goto

et al. 2001

J Cereb Blood Flow Metab

139

135

View full text Add to dashboard Cite

show abstract

“…Leptin-insensitive db/db mice have significantly smaller brains than control mice, accompanied by lower neuronal density and function [36, 37, 38]. Leptin also regulates brain development and the expression of neuronal and glial proteins [39, 40]such as growth-associated protein, syntaxin-1 and synaptosomal-associated protein-25 [40].…”

Section: Introductionmentioning

confidence: 99%

Leptin Immunoreactivity Is Localized to Neurons in Rat Brain

Ur¹,

Wilkinson²,

Morash³

et al. 2002

Neuroendocrinology

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Leptin is secreted from adipocytes and is thought to enter the brain to regulate and coordinate metabolism, feeding behaviour, energy balance and reproduction. It is now clear that there are many additional sites of leptin production, including human placenta, ovary, stomach, skeletal muscle, mammary gland, pituitary gland and brain. In the present work, we employed double-label immunofluorescent histochemistry to establish the neuronal localization of leptin immunoreactivity (IR). To accomplish this, we used the neuron-specific marker NeuN to label cells in the arcuate nucleus (ARC), piriform cortex and hippocampus. In the supraoptic nucleus (SON) and paraventricular nucleus (PVN), we used antisera to oxytocin and vasopressin as neuronal markers. Double labelling revealed leptin IR in neurons of the ARC and piriform cortex. Leptin IR was confined to the nucleus and to distinct perinuclear sites. In contrast, neurons in the CA 2/CA 3 region of the hippocampus showed little nuclear staining. Leptin IR was clustered around the nucleus in these cells. Neurons of the dentate gyrus exhibited both nuclear and perinuclear localization of leptin IR. In the SON/PVN, most oxytocin- and vasopressin-IR neurons also contained leptin IR, often in perinuclear sites. In conclusion, the neuronal, perinuclear localization of leptin IR in rat brain corresponds closely to that of leptin receptor (OB-R) IR, which has also been detected intracellularly. Our observation of leptin IR associated with cell nuclei suggests the existence of an OB-R distinct from the well-described membrane forms.

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Electrophysiological alterations of the central nervous system in diabetes mellitus

Mario

Valle²,

Pozzessere³

1995

Diabetes Metab. Rev.

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EL, and Lattimer SA: Complications: neuropathy, pathogenetic considerations. Diabetes Cure 15: Hansen S, and Ballantyne JP: Axonal dysfunction in the neuropathy of diabetes mellitus: a quantitative electrophysiological study. J Neurol Neurosurg Psychiatry 40: 555-564, 1977. Tackmann W, and Lehmann HS: Conduction of electrically elicited impulses in peripheral nerves of diabetic patients. Eur Neurol 19: 20-29, 1980. Halar EM, Graf RJ, Holter JB, Brozovich FV, and Soine TL: Diabetic neuropathy: a clinical, laboratory and electrodiagnostic study. Arch

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Unique alterations of neuropeptide content in median eminence, amygdala, and dorsal vagal complex of 3- and 6-week-old diabetes mutant mice

Cited by 10 publications

References 45 publications

Experimental Stroke in the Female Diabetic, db/db, Mouse

Experimental Stroke in the Female Diabetic, db/db, Mouse

Leptin Immunoreactivity Is Localized to Neurons in Rat Brain

Electrophysiological alterations of the central nervous system in diabetes mellitus

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