Page last updated: 2024-10-30

metformin and Progeria

metformin has been researched along with Progeria in 3 studies

Metformin: A biguanide hypoglycemic agent used in the treatment of non-insulin-dependent diabetes mellitus not responding to dietary modification. Metformin improves glycemic control by improving insulin sensitivity and decreasing intestinal absorption of glucose. (From Martindale, The Extra Pharmacopoeia, 30th ed, p289)
metformin : A member of the class of guanidines that is biguanide the carrying two methyl substituents at position 1.

Progeria: An abnormal congenital condition, associated with defects in the LAMIN TYPE A gene, which is characterized by premature aging in children, where all the changes of cell senescence occur. It is manifested by premature graying; hair loss; hearing loss (DEAFNESS); cataracts (CATARACT); ARTHRITIS; OSTEOPOROSIS; DIABETES MELLITUS; atrophy of subcutaneous fat; skeletal hypoplasia; elevated urinary HYALURONIC ACID; and accelerated ATHEROSCLEROSIS. Many affected individuals develop malignant tumors, especially SARCOMA.

Research Excerpts

ExcerptRelevanceReference
"Metformin has also recently been shown to beneficially alter gene splicing in normal humans."5.48Cellular stress and AMPK activation as a common mechanism of action linking the effects of metformin and diverse compounds that alleviate accelerated aging defects in Hutchinson-Gilford progeria syndrome. ( Finley, J, 2018)
"Metformin treatment partially restored normal nuclear phenotypes, delayed senescence, activated the phosphorylation of AMP-activated protein kinase and decreased reactive oxygen species formation in HGPS dermal fibroblasts."5.46Metformin alleviates ageing cellular phenotypes in Hutchinson-Gilford progeria syndrome dermal fibroblasts. ( Park, SK; Shin, OS, 2017)
"Metformin has also recently been shown to beneficially alter gene splicing in normal humans."1.48Cellular stress and AMPK activation as a common mechanism of action linking the effects of metformin and diverse compounds that alleviate accelerated aging defects in Hutchinson-Gilford progeria syndrome. ( Finley, J, 2018)
"Metformin treatment partially restored normal nuclear phenotypes, delayed senescence, activated the phosphorylation of AMP-activated protein kinase and decreased reactive oxygen species formation in HGPS dermal fibroblasts."1.46Metformin alleviates ageing cellular phenotypes in Hutchinson-Gilford progeria syndrome dermal fibroblasts. ( Park, SK; Shin, OS, 2017)

Research

Studies (3)

TimeframeStudies, this research(%)All Research%
pre-19900 (0.00)18.7374
1990's0 (0.00)18.2507
2000's0 (0.00)29.6817
2010's3 (100.00)24.3611
2020's0 (0.00)2.80

Authors

AuthorsStudies
Finley, J2
Park, SK1
Shin, OS1

Other Studies

3 other studies available for metformin and Progeria

ArticleYear
Cellular stress and AMPK activation as a common mechanism of action linking the effects of metformin and diverse compounds that alleviate accelerated aging defects in Hutchinson-Gilford progeria syndrome.
    Medical hypotheses, 2018, Volume: 118

    Topics: Aging; Alternative Splicing; AMP-Activated Protein Kinases; Animals; Cell Nucleus; Cellular Senescen

2018
Alteration of splice site selection in the LMNA gene and inhibition of progerin production via AMPK activation.
    Medical hypotheses, 2014, Volume: 83, Issue:5

    Topics: Alternative Splicing; AMP-Activated Protein Kinases; Animals; Berberine; DNA, Mitochondrial; Enzyme

2014
Metformin alleviates ageing cellular phenotypes in Hutchinson-Gilford progeria syndrome dermal fibroblasts.
    Experimental dermatology, 2017, Volume: 26, Issue:10

    Topics: AMP-Activated Protein Kinases; Animals; Cell Line; Cell Nucleus; Cell Proliferation; Cellular Senesc

2017