scholarly journals Sex differences in the effects of androgens acting in the central nervous system on metabolism

2016 ◽  
Vol 18 (4) ◽  
pp. 415-424 ◽  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Central Nervous System ◽  
Nervous System ◽  
Metabolic Regulation ◽  
Energy Homeostasis ◽  
Sexually Dimorphic ◽  
Metabolic Homeostasis ◽  
The Central Nervous System

One of the most sexually dimorphic aspects of metabolic regulation is the bidirectional modulation of glucose and energy homeostasis by testosterone in males and females. Testosterone deficiency predisposes men to metabolic dysfunction, with excess adiposity, insulin resistance, and type 2 diabetes, whereas androgen excess predisposes women to insulin resistance, adiposity, and type 2 diabetes. This review discusses how testosterone acts in the central nervous system, and especially the hypothalamus, to promote metabolic homeostasis or dysfunction in a sexually dimorphic manner. We compare the organizational actions of testosterone, which program the hypothalamic control of metabolic homeostasis during development, and the activational actions of testosterone, which affect metabolic function after puberty. We also discuss how the metabolic effect of testosterone is centrally mediated via the androgen receptor.

Measurement of the visual system response and its correlation with the central nervous system in patients diagnosed with type 2 diabetes mellitus (T2DM)

2020 ◽  
Vol 40 (4) ◽  
pp. 1499-1511
Author(s):  
José Alfredo Padilla Medina ◽  
Carlos Alonso Herrera Ramírez ◽  
Luz María Cardona Torres ◽  
Delia Angélica Galicia Reséndiz ◽  
Juan Prado Olivares ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Central Nervous System ◽  
Nervous System ◽  
Type 2 Diabetes Mellitus ◽  
Visual System ◽  
System Response ◽  
The Central Nervous System

scholarly journals Update in the CNS Response to Hypoglycemia

2012 ◽  
Vol 97 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Rory J. McCrimmon
Keyword(s):  
Type 2 Diabetes ◽  
Central Nervous System ◽  
Type 1 Diabetes ◽  
Nervous System ◽  
Animal Studies ◽  
Human Subjects ◽  
Diabetes Research ◽  
The Central Nervous System

Hypoglycemia remains a major clinical issue in the management of people with type 1 and type 2 diabetes. Research in basic science is only beginning to unravel the mechanisms that: 1) underpin the detection of hypoglycemia and initiation of a counterregulatory defense response; and 2) contribute to the development of defective counterregulation in both type 1 and type 2 diabetes, particularly after prior exposure to repeated hypoglycemia. In animal studies, the central nervous system has emerged as key to these processes. However, bench-based research needs to be translated through studies in human subjects as a first step to the future development of clinical intervention. This Update reviews studies published in the last 2 yr that examined the central nervous system effects of hypoglycemia in human subjects, largely through neuroimaging techniques, and compares these data with those obtained from animal studies and the implications for future therapies. Based on these studies, it is increasingly clear that our understanding of how the brain responds and adapts to recurrent hypoglycemia remains very limited. Current therapies have provided little evidence that they can prevent severe hypoglycemia or improve hypoglycemia awareness in type 1 diabetes. There remains an urgent need to increase our understanding of how and why defective counterregulation develops in type 1 diabetes in order for novel therapeutic interventions to be developed and tested.

Relation of insulin resistance to neurocognitive function and electroencephalography in obese children

2017 ◽  
Vol 30 (10) ◽  
Author(s):  
Onur Akın ◽  
İbrahim Eker ◽  
Mutluay Arslan ◽  
Süleyman Tolga Yavuz ◽  
Sevil Akman ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Central Nervous System ◽  
Nervous System ◽  
Healthy Children ◽  
Model Assessment ◽  
Obese Children ◽  
Neurocognitive Functions ◽  
The Central Nervous System ◽  
Biochemical Indices ◽  
The Impact

AbstractBackground:Childhood obesity may lead to neuronal impairment in both the peripheral and the central nervous system. This study aimed to investigate the impact of obesity and insulin resistance (IR) on the central nervous system and neurocognitive functions in children.Methods:Seventy-three obese children (38 male and 35 female) and 42 healthy children (21 male and 21 female) were recruited. Standard biochemical indices and IR were evaluated. The Wechsler Intelligence Scale for Children-Revised (WISC-R) and electroencephalography (EEG) were administered to all participants. The obese participants were divided into two groups based on the presence or absence of IR, and the data were compared between the subgroups.Results:Only verbal scores on the WISC-R in the IR+ group were significantly lower than those of the control and IR– groups. There were no differences between the groups with respect to other parameters of the WISC-R or the EEG. Verbal scores of the WISC-R were negatively correlated with obesity duration and homeostatic model assessment-insulin resistance (HOMA-IR) values. EEGs showed significantly more frequent ‘slowing during hyperventilation’ (SDHs) in obese children than non-obese children.Conclusions:Neurocognitive functions, particularly verbal abilities, were impaired in obese children with IR. An early examination of cognitive functions may help identify and correct such abnormalities in obese children.

Brain Glucose Sensing, Counterregulation, and Energy Homeostasis

Physiology ◽  
2007 ◽  
Vol 22 (4) ◽  
pp. 241-251 ◽  
Author(s):  
Nell Marty ◽  
Michel Dallaporta ◽  
Bernard Thorens
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Energy Homeostasis ◽  
Critical Role ◽  
Glucose Sensing ◽  
Neuronal Circuits ◽  
Brain Glucose ◽  
The Central Nervous System

Neuronal circuits in the central nervous system play a critical role in orchestrating the control of glucose and energy homeostasis. Glucose, beside being a nutrient, is also a signal detected by several glucose-sensing units that are located at different anatomical sites and converge to the hypothalamus to cooperate with leptin and insulin in controlling the melanocortin pathway.

Development and regeneration in the central nervous system

1990 ◽  
Vol 327 (1239) ◽  
pp. 127-143 ◽  
Keyword(s):  
Stem Cells ◽  
Central Nervous System ◽  
Nervous System ◽  
Progenitor Cells ◽  
Progenitor Cell ◽  
Cell Types ◽  
The Central Nervous System

As part of our attempts to understand principles that underly organism development, we have been studying the development of the rat optic nerve. This simple tissue is composed of three glial cell types derived from two distinct cellular lineages. Type-1 astrocytes appear to be derived from a monopotential neuroepithelial precursor, whereas type-2 astrocytes and oligodendrocytes are derived from a common oligodendrocyte-type-2 astrocyte (O-2A) progenitor cell. Type-1 astrocytes modulate division and differentiation of O-2A progenitor cells through secretion of platelet-derived growth factor, and can themselves be stimulated to divide by peptide mitogens and through stimulation of neurotransmitter receptors. In vitro analysis indicates that many dividing O-2A progenitors derived from optic nerves of perinatal rats differentiate symmetrically and clonally to give rise to oligodendrocytes, or can be induced to differentiate into type-2 astrocytes. O-2A perinatal progenitors can also differentiate to form a further O-2A lineage cell, the O-2A adult progenitor, which has properties specialized for the physiological requirements of the adult nervous system. In particular, O-2A adult progenitors have many of the features of stem cells, in that they divide slowly and asymmetrically and appear to have the capacity for extended self-renewal. The apparent derivation of a slowly and asymmetrically dividing cell, with properties appropriate for homeostatic maintenance of existing populations in the mature animal, from a rapidly dividing cell with properties suitable for the rapid population and myelination of central nervous system (CNS) axon tracts during early development, offers novel and unexpected insights into the possible origin of self-renewing stem cells and also into the role that generation of stem cells may play in helping to terminate the explosive growth of embryogenesis. Moreover, the properties of O-2A adult progenitor cells are consistent with, and may explain, the failure of successful myelin repair in conditions such as multiple sclerosis, and thus seem to provide a cellular biological basis for understanding one of the key features of an important human disease.

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