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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sexual behavior is a constituent of the reproductive function of the organism. In sexually mature individuals the synchronization of the level of sexual activity with the reaction of the hypothalamo-hypophyseo-gonadal system to the relevant environmental stimuli is a necessary condition for the preservation of the species. In this context, the study of the neuroendocrine mechanisms shaping a specific level of activity of sexual behavior is an important problem for investigators. The dependence of the level of sexual activity on the integrity of certain CNS structures (first of all, the olfactory bulbs, amygdala, hypothalamus, and hypophysis) has been established. It has been demonstrated that label sex steroids accumulate selectively, and the regulation of the function of the gonads on the negative feedback principle is also accomplished in these regions precisely. In addition to the participation of the sex steroids in the formation of a specific level of sexual activity, an important role has been established at the present time for luliberin (LHRH) producing system and the neurotransmitters. The stability of the functioning of the reproductive system depends on a multiplicity of factors of the internal and external milieu. Serious disturbances in its function are associated with the alteration in carbohydrate homeostasis underlying a disease such as diabetes mellitus. This is manifested in a reduction in the weight of the accessory sex glands, steroidogenic activity and spermatogenesis, in a change in the secretion of gonadotropins, as well as in a diminution of fertility and sexual behavior.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Disturbance of neuroendocrine regulation of sexual behavior of male rats with streptozotocin diabetes. 829 33

Olfactory dysfunction has been reported in individuals with diabetes mellitus, but the etiology is unknown. Diabetes is often complicated by serious medical conditions which could be related to the development of decreased olfactory ability. Overall, our 111 subjects with diabetes showed deficiencies in their ability to identify odorants measured with the Odorant Confusion Matrix (mean = 67.8% correct). The presence of macrovascular disease was found to be associated with olfactory dysfunction. Glycemic control as well as the type and duration of diabetes were not related to olfactory ability. Also, there was no distinct association with the presence of neuropathy, retinopathy, nephropathy, hypertension, or impotence. Consistent with previous studies utilizing measures of odorant identification, performance decreased with increased age, females were somewhat superior to males, and smoking had a deleterious effect. Other nondiabetes-related medical conditions and medications had no apparent effect on the olfactory ability of our subjects. These results suggest that the sequelae associated with macrovascular disease, such as perhaps, ischemia, to the olfactory area, impact negatively on olfactory ability.
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PMID:Olfactory dysfunction in diabetes mellitus. 843 58

Alzheimer disease is characterized by the presence of beta-amyloid protein deposits, neurofibrillary tangles and cholinergic dysfunction throughout the hippocampal region. In addition, the hippocampus, hypothalamus and olfactory bulb--the three areas where the insulin receptors are most dense--are also subject to neurodegeneration. The exact cause of the beta-amyloid deposits and NFTs is unknown. However, it is our intention to explicate the various pathogenic pathways through which Alzheimer disease arises. Fundamentally, the structural and metabolic damage found in Alzheimer disease is due to sustained elevation of interleukin-1 beta, a feature which is also found in insulin-dependent diabetes mellitus. Similarly, the beta-AP deposits found in the Alzheimer brain share the same molecular structure as the amylin deposits found in the pancreatic beta-cells in non-insulin-dependent diabetes mellitus (NIDDM), and are equally neurotoxic. These, and other pathophysiological parallels, afford some insight into the probably cause of Alzheimer disease and, as such, forms the basis of the causal hypothesis advanced in this paper.
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PMID:Interleukin-1 beta: a common cause of Alzheimer's disease and diabetes mellitus. 877 Oct 51

We report a patient with chronic active hepatitis C developing acute anosmia during interferon (IFN) therapy. On July 31, he began receiving 6 MU of IFN-alpha daily. On September 26, he failed to smell gas leaking from a gas cooker, so IFN therapy was discontinued. He showed no reaction on a standard olfactory acuity test. As the patient had borderline diabetes, the association of anosmia with impaired glucose tolerance cannot completely be excluded, but his anosmia was probably induced by IFN therapy, since anosmia developed 10 days after the initiation of the IFN therapy, without any deterioration of his glucose intolerance.
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PMID:Interferon-induced anosmia in a patient with chronic hepatitis C. 944 93

Diabetes is often complicated by serious medical conditions which could be related to the development of auditory system and cranial nerves lesions, disorder of sound localisation and decreased olfactory and taste ability. Cranial nerve palsies in diabetes are considered as an integral part of the main disease. Twenty nine children with diabetes and non-diabetics control group, without a history of exposure to noise, ototoxic drugs, or ear disease aged 4-19 years old were examined. Hearing impairment may be present in children with disease duration above 3-5 years and in children with other complications. Sound localisation tests were performed by the method of Zakrzewski from a free auditory field, measuring the angle of directional hearing acuity in 35 diabetics age from 16 to 78 years. Longer duration of diabetes was associated with higher directional hearing acuity. Higher hearing loss was observed with higher directional values in diabetics. The authors investigated smell and taste in 35 diabetics. All patients were treated with insulin. Impairment value of smell identification thresholds was much more frequent than impairment of smell perception. In no case raised threshold of taste perception.
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PMID:[Hearing loss, disorders of sound localization with the preservation ofsmell and taste in diabetics]. 1068 13

This case details a patient with primary amenorrhea with an unusual cause. She presented at age 16 with short stature, minimal sexual development and no prior menses. Her history was significant for poorly controlled type 1 diabetes. She had been evaluated previously for growth hormone deficiency, and had received a short course of growth hormone therapy. Of greatest significance was the fact that she had also had a decreased sense of smell since her youth. Although a previous computerized tomography scan had been reported as normal, follow-up magnetic resonance imaging demonstrated the absence of olfactory bulbs. Smell testing confirmed the absence of smell and testing of gonadotropin releasing hormone demonstrated an inadequate response. All of these features suggested Kallmann syndrome. This syndrome commonly presents with delayed onset of puberty and decreased or absent sense of smell. There are also many associated features, and the disease is remarkable for its great genotypic and phenotypic variability. Current understanding of its pathogenesis, the commonly associated features of Kallmann syndrome and the impact of diabetes on growth and sexual development are reviewed.
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PMID:A case of primary amenorrhea, diabetes and anosmia. 1081 10

The brain contains a subpopulation of glucosensing neurons that alter their firing rate in response to elevated glucose concentrations. In pancreatic beta-cells, glucokinase (GK), the rate-limiting enzyme in glycolysis, mediates glucose-induced insulin release by regulating intracellular ATP production. A similar role for GK is proposed to underlie neuronal glucosensing. Via in situ hybridization, GK mRNA was localized to hypothalamic areas that are thought to contain relatively large populations of glucosensing neurons (the arcuate, ventromedial, dorsomedial, and paraventricular nuclei and the lateral area). GK also was found in brain areas without known glucosensing neurons (the lateral habenula, the bed nucleus stria terminalis, the inferior olive, the retrochiasmatic and medial preoptic areas, and the thalamic posterior paraventricular, interpeduncular, oculomotor, and anterior olfactory nuclei). Conversely, GK message was not found in the nucleus tractus solitarius, which contains glucosensing neurons, or in ependymal cells lining the third ventricle, where others have described its presence. In the arcuate nucleus, >75% of neuropeptide Y-positive neurons also expressed GK, and most GK+ neurons also expressed KIR6.2 (the pore-forming subunit of the ATP-sensitive K+ channel). The anatomic distribution of GK mRNA was confirmed in micropunch samples of hypothalamus via reverse transcription-polymerase chain reaction (RT-PCR). Nucleotide sequencing of the recovered PCR product indicated identity with nucleotides 1092-1411 (within exon 9 and 10) of hepatic and beta-cell GK. The specific anatomic localization of GK mRNA in hypothalamic areas known to contain glucosensing neurons and the coexpression of KIR6.2 and NPY in GK+ neurons support a role for GK as a primary determinant of glucosensing in neuropeptide neurons that integrate multiple signals relating to peripheral energy metabolism.
Diabetes 2000 May
PMID:Localization of glucokinase gene expression in the rat brain. 1090 75

Wolfram (DIDMOAD) syndrome is an autosomal recessive neurodegenerative disorder accompanied by insulin-dependent diabetes mellitus and progressive optic atrophy. Recent positional cloning led to identification of the WFS1 (Wolfram syndrome 1) gene, a member of a novel gene family of unknown function. In this study, we generated a specific antibody against the C-terminus of the WFS1 protein and investigated its subcellular localization in cultured cells. We also studied its distribution in the rat brain. Biochemical studies indicated the WFS1 protein to be an integral, endoglycosidase H-sensitive membrane glycoprotein that localizes primarily in the endoplasmic reticulum (ER). Consistent with this, immunofluorescence cell staining of overexpressed WFS1 showed a characteristic reticular pattern over the cytoplasm and overlapped with the ER marker staining. No co-localization of WFS1 with mitochondria argues against an earlier clinical hypothesis that Wolfram syndrome is a mitochondria-mediated disorder. In the rat brain, at both the protein and mRNA level, WFS1 was found to be present predominantly in selected neurons in the hippocampus CA1, amygdaloid areas, olfactory tubercle and superficial layer of the allocortex. These expression sites, i.e. components of the limbic system or structures closely associated with this system, may be involved in the psychiatric, behavioral and emotional abnormalities characteristic of this syndrome. ER localization of WFS1 suggests that this protein plays an as yet undefined role in membrane trafficking, protein processing and/or regulation of ER calcium homeostasis. These studies represent a first step toward the characterization of WFS1 protein, which presumably functions to maintain certain populations of neuronal and endocrine cells.
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PMID:WFS1 (Wolfram syndrome 1) gene product: predominant subcellular localization to endoplasmic reticulum in cultured cells and neuronal expression in rat brain. 1118 71

Insulin and its receptor are found throughout the central nervous system (CNS). Insulin administered into the CNS can exert powerful effects, yet the consensus is that little or no insulin is produced in the CNS. Therefore, CNS insulin is essentially dependent on the ability of peripheral insulin to cross the blood-brain barrier (BBB). Insulin is known to cross the BBB by a saturable transport mechanism. This transporter shows some thematic similarities to other transporters for peptides or regulatory proteins. It is unevenly distributed throughout the CNS with the olfactory bulbs having the fastest transport rate of any brain region. It is partially saturated at euglycemic levels, suggesting that its main signaling function occurs at physiological blood levels, rather than as a brake to hypoglycemic events. One probable function of the BBB transporter is to allow CNS insulin to act as a counter-regulatory hormone to peripheral insulin. The transporter is regulated, with the transport rate of insulin being altered during development and by fasting, obesity, hibernation, diabetes mellitus and Alzheimer's disease. Enhancement of insulin transport by lipopolysaccharide could be the basis for the insulin resistance seen with bacterial infections. Inhibition of insulin transport across the BBB by dexamethasone could be the basis for the enhanced appetite seen with glucocorticoid treatments. Insulin itself also has effects on the BBB, altering enzymatic and transporter functions. Overall, BBB transport of insulin provides a mechanism for peripheral insulin to act within the CNS as a regulatory peptide.
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PMID:The source of cerebral insulin. 1509 69

The increased incidence of Type I and Type II diabetes among adults and adolescents is a growing public health concern worldwide. The primary objective of diabetes mellitus management involves keeping glycemia levels within the euglycemic range to prevent a variety of serious health complications. Unfortunately, daily self-monitoring is both a requirement and a problem for many patients with diabetes, particularly children and adolescents. Studies have shown that as many as 43% of adolescents and 30% of children (<14 years old) regularly forget to use glycemic tests and are significantly poorer at recognizing and reporting symptoms and signs of hypoglycemia/hyperglycemia. For this reason, methods for noninvasive, continuous monitoring that can signal glycemic status to a parent, teacher, or other caregiver would improve the care and management of symptoms of diabetes among these individuals. The goal of this review is to describe and evaluate electronic olfaction technology ("electronic nose") for monitoring the presence and levels of volatile chemicals from human body and breath that can be used to evaluate status of diabetes. The review is organized in four sections. The first section reviews the chemistry of the volatile signals that are produced by the body that are indicative of metabolic status. The second section provides an overview of novel sensor technology, e.g., "electronic olfaction," that mimics the biological olfactory system and can be used to monitor and identify complex plumes of volatiles that are signatures of metabolic states. The third section reviews studies that have employed electronic "nose" technology for diagnosis and monitoring of diabetes via urine and breath, and the final section discusses needed future directions for the development of olfactory-based metabolic monitoring, particularly among noncompliant populations.
Diabetes Technol Ther 2004 Aug
PMID:Volatile metabolic monitoring of glycemic status in diabetes using electronic olfaction. 1532 Oct 12


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