scholarly journals Growth Hormone and IGF1 Actions in Kidney Development and Function

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3371
Author(s):  
Evgenia Gurevich ◽  
Yael Segev ◽  
Daniel Landau
Keyword(s):  
Growth Hormone ◽  
Kidney Development ◽  
Transgenic Animal ◽  
Calcium Handling ◽  
Normal Kidney ◽  
Kidney Hypertrophy ◽  
Transgenic Animal Models ◽  
And Function ◽  
Rhgh Treatment ◽  
Gh Excess

Growth hormone (GH) exerts multiple effects on different organs including the kidneys, either directly or via its main mediator, insulin-like-growth factor-1 (IGF-1). The GH/IGF1 system plays a key role in normal kidney development, glomerular hemodynamic regulation, as well as tubular water, sodium, phosphate, and calcium handling. Transgenic animal models demonstrated that GH excess (and not IGF1) may lead to hyperfiltration, albuminuria, and glomerulosclerosis. GH and IGF-1 play a significant role in the early development of diabetic nephropathy, as well as in compensatory kidney hypertrophy after unilateral nephrectomy. Chronic kidney disease (CKD) and its complications in children are associated with alterations in the GH/IGF1 axis, including growth retardation, related to a GH-resistant state, attributed to impaired kidney postreceptor GH-signaling and chronic inflammation. This may explain the safety of prolonged rhGH-treatment of short stature in CKD.

scholarly journals The Role of the Growth Hormone/Insulin-Like Growth Factor System in Visceral Adiposity

2017 ◽  
Vol 10 ◽  
pp. 117862641770399 ◽  
Author(s):  
Moira S Lewitt
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Visceral Obesity ◽  
Transgenic Animal ◽  
Visceral Adiposity ◽  
Future Research ◽  
Insulin Like Growth Factor ◽  
Igf System ◽  
Proliferation And Differentiation ◽  
Transgenic Animal Models

There is substantial evidence that the growth hormone (GH)/insulin-like growth factor (IGF) system is involved in the pathophysiology of obesity. Both GH and IGF-I have direct effects on adipocyte proliferation and differentiation, and this system is involved in the cross-talk between adipose tissue, liver, and pituitary. Transgenic animal models have been of importance in identifying mechanisms underlying these interactions. It emerges that this system has key roles in visceral adiposity, and there is a rationale for targeting this system in the treatment of visceral obesity associated with GH deficiency, metabolic syndrome, and lipodystrophies. This evidence is reviewed, gaps in knowledge are highlighted, and recommendations are made for future research.

Effects of long-term elevated serum levels of growth hormone on life expectancy of mice: Lessons from transgenic animal models

1993 ◽  
Vol 68 (1-3) ◽  
pp. 71-87 ◽  
Author(s):  
Eckhard Wolf ◽  
Eva Kahnt ◽  
Jörn Ehrlein ◽  
Walter Hermanns ◽  
Gottfried Brem ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Animal Models ◽  
Life Expectancy ◽  
Elevated Serum ◽  
Serum Levels ◽  
Transgenic Animal ◽  
Transgenic Animal Models

scholarly journals Apparently normal kidney development in mice with conditional disruption of ANG II-AT1 receptor genes in FoxD1-positive stroma cell precursors

2019 ◽  
Vol 316 (6) ◽  
pp. F1191-F1200 ◽  
Author(s):  
Julia Schrankl ◽  
Bjoern Neubauer ◽  
Michaela Fuchs ◽  
Katharina Gerl ◽  
Charlotte Wagner ◽  
...  
Keyword(s):  
Kidney Development ◽  
Receptor Gene ◽  
Cell Lineage ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Cell Types ◽  
Ang Ii ◽  
Normal Kidney ◽  
And Function

An intact renin-angiotensin system involving ANG II type 1 (AT1) receptors is crucial for normal kidney development. It is still unclear in which cell types AT1 receptor signaling is required for normal kidney development, maturation, and function. Because all kidney cells deriving from stroma progenitor cells express AT1 receptors and because stromal cells fundamentally influence nephrogenesis and tubular maturation, we investigated the relevance of AT1 receptors in stromal progenitors and their descendants for renal development and function. For this aim, we generated and analyzed mice with conditional deletion of AT1A receptor in the FoxD1 cell lineage in combination with global disruption of the AT1B receptor gene. These FoxD1-AT1ko mice developed normally. Their kidneys showed neither structural nor functional abnormalities compared with wild-type mice, whereas in isolated perfused FoxD1-AT1ko kidneys, the vasoconstrictor and renin inhibitory effects of ANG II were absent. In vivo, however, plasma renin concentration and renal renin expression were normal in FoxD1-AT1ko mice, as were blood pressure and glomerular filtration rate. These findings suggest that a strong reduction of AT1 receptors in renal stromal progenitors and their descendants does not disturb normal kidney development.

scholarly journals A SELECTION OF TRANSGENIC ANIMAL MODELS USED IN BIOMEDICAL RESEARCH

2013 ◽  
Vol 2 ◽  
Author(s):  
Hussein Ramadan ◽  
Kristopher Grohn ◽  
Adel Mohamed
Keyword(s):  
Animal Models ◽  
Transgenic Animal ◽  
Structure Design ◽  
Transgenic Technology ◽  
Autoimmune Encephalomyelitis ◽  
Transgenic Animal Models ◽  
Living Organisms ◽  
And Function ◽  
Micro Organisms ◽  
Selection Of

The term transgenic animal refers to an animal whose genetic composition has been altered by an addition of foreign DNA. The introduced DNA is called a transgene and the overall process is called transgenic technology. These terms now include the use of living organisms or their parts to make or modify products, to change the characteristics of plants or animals, or to develop micro-organisms forspecific uses that currently include several plants and a number of animal species. During the last two decades, transgenic animal model has been an essential mainstay tool in refining our understanding to gene regulation and function of both biological systems and human diseases. The aims of this review article are 1) to elaborate on how transgenic technology is being used to develop the next genera-tion of animal models and 2) to provide an update of the recent advances and a possible structure design for future studies. This review covers the most used animal models of some human disease and specifically discusses two studies conducted on a mouse model of experimental autoimmune encephalomyelitis (EAE) that reproduced specific features of the histopathology and neurobiology ofMultiple Sclerosis (MS). This report is presented with the hope to provide both educational and practical basis for the use of these informative animal models.

scholarly journals Calcineurin A-α But Not A-β Is Required for Normal Kidney Development and Function

2004 ◽  
Vol 165 (5) ◽  
pp. 1755-1765 ◽  
Author(s):  
Jennifer L. Gooch ◽  
Juan J. Toro ◽  
Rebecca L. Guler ◽  
Jeffrey L. Barnes
Keyword(s):  
Kidney Development ◽  
Normal Kidney ◽  
Calcineurin A ◽  
And Function

scholarly journals Transgenic animal models of tauopathies

2005 ◽  
Vol 1739 (2-3) ◽  
pp. 251-259 ◽  
Author(s):  
Virginia M.-Y. Lee ◽  
Theresa K. Kenyon ◽  
John Q. Trojanowski
Keyword(s):  
Animal Models ◽  
Transgenic Animal ◽  
Transgenic Animal Models

Physical exercise increases autophagic signaling through ULK1 in human skeletal muscle

2015 ◽  
Vol 118 (8) ◽  
pp. 971-979 ◽  
Author(s):  
Andreas Buch Møller ◽  
Mikkel Holm Vendelbo ◽  
Britt Christensen ◽  
Berthil Forrest Clasen ◽  
Ann Mosegaard Bak ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Physical Exercise ◽  
Light Chain ◽  
Human Skeletal Muscle ◽  
Transgenic Animal ◽  
Dependent Manner ◽  
Healthy Humans ◽  
Transgenic Animal Models ◽  
Exercise Induced

Data from transgenic animal models suggest that exercise-induced autophagy is critical for adaptation to physical training, and that Unc-51 like kinase-1 (ULK1) serves as an important regulator of autophagy. Phosphorylation of ULK1 at Ser555 stimulates autophagy, whereas phosphorylation at Ser757 is inhibitory. To determine whether exercise regulates ULK1 phosphorylation in humans in vivo in a nutrient-dependent manner, we examined skeletal muscle biopsies from healthy humans after 1-h cycling exercise at 50% maximal O2 uptake on two occasions: 1) during a 36-h fast, and 2) during continuous glucose infusion at 0.2 kg/h. Physical exercise increased ULK1 phosphorylation at Ser555 and decreased lipidation of light chain 3B. ULK1 phosphorylation at Ser555 correlated positively with AMP-activated protein kinase-α Thr172 phosphorylation and negatively with light chain 3B lipidation. ULK1 phosphorylation at Ser757 was not affected by exercise. Fasting increased ULK1 and p62 protein expression, but did not affect exercise-induced ULK1 phosphorylation. These data demonstrate that autophagy signaling is activated in human skeletal muscle after 60 min of exercise, independently of nutritional status, and suggest that initiation of autophagy constitutes an important physiological response to exercise in humans.

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