Insulin II gene expression in rat central nervous system

Devaskar, Sherin U.; Singh, Bindya S.; Carnaghi, Lynn R.; Rajakumar, Premeela A.; Giddings, Stephen J.

doi:10.1016/0167-0115(93)90335-6

Cited by 129 publications

(76 citation statements)

References 13 publications

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“…These results show that the conversion efficiency of insulin-expressing cells remained low in these basic cultures. Insulin I is expressed not only by pancreas, but also by yolk sac [1,3,4] and fetal liver [3]. The fact that most insulin or C-peptide + cells in S EB-derived cells coexpress glucagon indicates that they are not yolk sac related, because this tissue does not express glucagon [6].…”

Section: Emergence Of Insulin I-expressing Cells In Tertiary Culturementioning

confidence: 99%

“…Neuronal cells [2] express only insulin II, whereas pancreas expresses both insulin I and II. Fetal liver and yolk sac, which lack the expression of glucagon [6], express predominately insulin II [3]. Insulin I is also expressed in fetal liver and yolk sac but at much lower levels [3,4].…”

Section: Introductionmentioning

confidence: 99%

“…Fetal liver and yolk sac, which lack the expression of glucagon [6], express predominately insulin II [3]. Insulin I is also expressed in fetal liver and yolk sac but at much lower levels [3,4]. The transcription factor pdx-1 is essential for the earliest stage of pancreatic development [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

“…A potential source for endocrine stem cells is embryonic stem (ES) cells. Because of their unlimited proliferation and differentiation potentials, ES cells are considered an important source for cell therapies targeted to several diseases, including diabetes.There are two nonallelic insulin genes (insulin I and II) expressed in multiple sites in mice during development [1][2][3][4][5][6][7] …”

mentioning

confidence: 99%

“…There are two nonallelic insulin genes (insulin I and II) expressed in multiple sites in mice during development [1][2][3][4][5][6][7] …”

mentioning

confidence: 99%

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Committing Embryonic Stem Cells to Early Endocrine Pancreas In Vitro

et al. 2004

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Type I diabetes is marked by a deficiency of endocrine β cells in the pancreatic islets of Langerhans. Daily injection of insulin is the current treatment for the disease. Because insulin injection cannot match the precise timing and dosing of physiological secretion of insulin by islets in response to hyperglycemia, severe side effects develop over time. Transplantation of islets represents a potential cure; however, limitations on the availability of cadaveric organs restrict this procedure to only a small percentage of patients. Pancreatic endocrine stem cells exist in the developing embryonic pancreas. The isolation, expansion, and differentiation of pancreatic endocrine stem cells would provide an unlimited source of islet cells for transplantation and treatment for type I diabetes. A potential source for endocrine stem cells is embryonic stem (ES) cells. Because of their unlimited proliferation and differentiation potentials, ES cells are considered an important source for cell therapies targeted to several diseases, including diabetes.There are two nonallelic insulin genes (insulin I and II) expressed in multiple sites in mice during development [1][2][3][4][5][6][7] Abstract A panel of genetic markers was used to assess the in vitro commitment of murine embryonic stem (ES) cells toward the endoderm-derived pancreas and to distinguish insulin-expressing cells of this lineage from other lineagessuch as neuron, liver, and yolk sac. There are two nonallelic insulin genes in mice. Neuronal cells express only insulin II, whereas the pancreas expresses both insulin I and II. Yolk sac and fetal liver express predominately insulin II, small amounts of insulin I, and no glucagon. We found that ES-derived embryoid bodies cultured in the presence of stage-specific concentrations of monothioglycerol and 15% fetal calf serum, followed by serum-free conditions, give rise to a population that expresses insulin I, insulin II, pdx-1 (a pancreas marker), and Sox17 (an endoderm marker). Immunohistochemical staining shows intracellular insulin particles, and its de novo production was confirmed by staining for C-peptide. Most, but not all, of the insulin + or C-peptide + cells coexpress glucagon, demonstrating a differentiation pathway to pancreas rather than yolk sac or fetal liver. Addition of β-cell specification and differentiation factors activin βB, nicotinamide, and exendin-4 to later-stage culture increased insulin-positive cells to 2.73% of the total population, compared with the control culture, which gave rise to less than 1% insulin-staining cells. These findings suggest that stepwise culture manipulations can direct ES cells to become early endocrine pancreas.

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Section: Emergence Of Insulin I-expressing Cells In Tertiary Culturementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

“…There are two nonallelic insulin genes (insulin I and II) expressed in multiple sites in mice during development [1][2][3][4][5][6][7] …”

mentioning

confidence: 99%

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Committing Embryonic Stem Cells to Early Endocrine Pancreas In Vitro

et al. 2004

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Dietary restriction alters insulin signaling pathway in the brain

Todorovic,

Simeunovic,

Prvulovic

et al. 2023

BioFactors

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Insulin is known to be a key hormone in the regulation of peripheral glucose homeostasis, but beyond that, its effects on the brain are now undisputed. Impairments in insulin signaling in the brain, including changes in insulin levels, are thought to contribute significantly to declines in cognitive performance, especially during aging. As one of the most widely studied experimental interventions, dietary restriction (DR) is considered to delay the neurodegenerative processes associated with aging. Recently, however, data began to suggest that the onset and duration of a restrictive diet play a critical role in the putative beneficial outcome. Because the effects of DR on insulin signaling in the brain have been poorly studied, we decided to examine the effects of DR that differed in onset and duration: long‐term DR (LTDR), medium‐term DR (MTDR), and short‐term DR (STDR) on the expression of proteins involved in insulin signaling in the hippocampus of 18‐ and 24‐month‐old male Wistar rats. We found that DR‐induced changes in insulin levels in the brain may be independent of what happens in the periphery after restricted feeding. Significantly changed insulin content in the hippocampus, together with altered insulin signaling were found under the influence of DR, but the outcome was highly dependent on the onset and duration of DR.

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Central Regulation of Glucose Homeostasis

Tups¹,

Benzler²,

Sergi³

et al. 2017

Comprehensive Physiology

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The ability of the brain to directly control glucose levels in the blood independently of its effects on food intake and body weight has been known ever since 1854 when Claude Bernard, a French physiologist, discovered that lesioning the floor of the fourth ventricle in rabbits led to a rise of sugar in the blood. Despite this outstanding discovery at that time, it took more than 140 years before progress started to be made in identifying the underlying mechanisms of brain-mediated control of glucose homeostasis. Technological advances including the generation of brain insulin receptor null mice revealed that insulin action specifically in the central nervous system is required for the regulation of glucose metabolism, particularly in the modulation of hepatic glucose production. Furthermore, it was established that the hormone leptin, known for its role in regulating food intake and body weight, actually exerts its most potent effects on glucose metabolism, and that this function of leptin is mediated centrally. Under certain circumstances, high levels of leptin can replicate the actions of insulin, thus challenging the idea that life without insulin is impossible. Disruptions of central insulin signaling and glucose metabolism not only lead to impairments in whole body glucose homeostasis, they also have other serious consequences, including the development of Alzheimer's disease which is sometimes referred to as type 3 diabetes reflecting its common etiology with type 2 diabetes. © 2017 American Physiological Society. Compr Physiol 7:471-764, 2017.

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Insulin II gene expression in rat central nervous system

Cited by 129 publications

References 13 publications

Committing Embryonic Stem Cells to Early Endocrine Pancreas In Vitro

Committing Embryonic Stem Cells to Early Endocrine Pancreas In Vitro

Dietary restriction alters insulin signaling pathway in the brain

Central Regulation of Glucose Homeostasis

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