scholarly journals Diabetes Mellitus: Disorder of Cellular Dysfunction Due to Lack of Entry into Cell of Glucose. The Most Efficient Fuel for Cellular Function*

2021 ◽  
Vol 11 (03) ◽  
pp. 79-101
Author(s):  
Udaya M. Kabadi
Keyword(s):  
Diabetes Mellitus ◽  
Cellular Function ◽  
Cellular Dysfunction

scholarly journals Sphingolipid regulators of cellular dysfunction in Type 2 diabetes mellitus: a systems overview

2014 ◽  
Vol 9 (5) ◽  
pp. 553-569 ◽  
Author(s):  
Jessica S Ross ◽  
Sarah B Russo ◽  
Georgia C Chavis ◽  
Lauren A Cowart
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Cellular Dysfunction

scholarly journals Stress-induced RNA–chromatin interactions promote endothelial dysfunction

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Riccardo Calandrelli ◽  
Lixia Xu ◽  
Yingjun Luo ◽  
Weixin Wu ◽  
Xiaochen Fan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Diabetes Mellitus ◽  
Healthy Donor ◽  
Gene Network ◽  
Rna Seq ◽  
Dna Interactions ◽  
Chromatin Interactions ◽  
The Common ◽  
Induced Changes ◽  
Cellular Dysfunction

Abstract Chromatin-associated RNA (caRNA) has been proposed as a type of epigenomic modifier. Here, we test whether environmental stress can induce cellular dysfunction through modulating RNA-chromatin interactions. We induce endothelial cell (EC) dysfunction with high glucose and TNFα (H + T), that mimic the common stress in diabetes mellitus. We characterize the H + T-induced changes in gene expression by single cell (sc)RNA-seq, DNA interactions by Hi-C, and RNA-chromatin interactions by iMARGI. H + T induce inter-chromosomal RNA-chromatin interactions, particularly among the super enhancers. To test the causal relationship between H + T-induced RNA-chromatin interactions and the expression of EC dysfunction-related genes, we suppress the LINC00607 RNA. This suppression attenuates the expression of SERPINE1, a critical pro-inflammatory and pro-fibrotic gene. Furthermore, the changes of the co-expression gene network between diabetic and healthy donor-derived ECs corroborate the H + T-induced RNA-chromatin interactions. Taken together, caRNA-mediated dysregulation of gene expression modulates EC dysfunction, a crucial mechanism underlying numerous diseases.

Peer Relationship Problems in Children with Tourette's Disorder or Diabetes Mellitus

1998 ◽  
Vol 39 (5) ◽  
pp. 663-668 ◽  
Author(s):  
Harry N. Bawden ◽  
Aidan Stokes ◽  
Carol S. Camfield ◽  
Peter R. Camfield ◽  
Sonia Salisbury
Keyword(s):  
Diabetes Mellitus ◽  
Peer Relationship ◽  
Tourette’S Disorder ◽  
Relationship Problems ◽  
Tourette's Disorder

Intramuscular Nerve and Neuromuscular Junction Alteration In Extraocular Muscles of Diabetic Mice

1985 ◽  
Vol 43 ◽  
pp. 682-683
Author(s):  
Bruce R. Pachter
Keyword(s):  
Diabetes Mellitus ◽  
Peripheral Nerves ◽  
Sudden Onset ◽  
Extraocular Muscles ◽  
Diabetic Patients ◽  
Oculomotor Palsy ◽  
Third Nerve Palsy ◽  
Patients With Diabetes ◽  
Intramuscular Nerve ◽  
Oculomotor Nerves

Diabetes mellitus is one of the commonest causes of neuropathy. Diabetic neuropathy is a heterogeneous group of neuropathic disorders to which patients with diabetes mellitus are susceptible; more than one kind of neuropathy can frequently occur in the same individual. Abnormalities are also known to occur in nearly every anatomic subdivision of the eye in diabetic patients. Oculomotor palsy appears to be common in diabetes mellitus for their occurrence in isolation to suggest diabetes. Nerves to the external ocular muscles are most commonly affected, particularly the oculomotor or third cranial nerve. The third nerve palsy of diabetes is characteristic, being of sudden onset, accompanied by orbital and retro-orbital pain, often associated with complete involvement of the external ocular muscles innervated by the nerve. While the human and experimental animal literature is replete with studies on the peripheral nerves in diabetes mellitus, there is but a paucity of reported studies dealing with the oculomotor nerves and their associated extraocular muscles (EOMs).

Autophagy and ageing: implications for age-related neurodegenerative diseases

2013 ◽  
Vol 55 ◽  
pp. 119-131 ◽  
Author(s):  
Bernadette Carroll ◽  
Graeme Hewitt ◽  
Viktor I. Korolchuk
Keyword(s):  
Neurodegenerative Diseases ◽  
Energy Availability ◽  
Future Studies ◽  
Intracellular Degradation ◽  
Age Related ◽  
Autophagy Induction ◽  
Social Importance ◽  
Cellular Dysfunction ◽  
Autophagy Activity ◽  
Intense Research

Autophagy is a process of lysosome-dependent intracellular degradation that participates in the liberation of resources including amino acids and energy to maintain homoeostasis. Autophagy is particularly important in stress conditions such as nutrient starvation and any perturbation in the ability of the cell to activate or regulate autophagy can lead to cellular dysfunction and disease. An area of intense research interest is the role and indeed the fate of autophagy during cellular and organismal ageing. Age-related disorders are associated with increased cellular stress and assault including DNA damage, reduced energy availability, protein aggregation and accumulation of damaged organelles. A reduction in autophagy activity has been observed in a number of ageing models and its up-regulation via pharmacological and genetic methods can alleviate age-related pathologies. In particular, autophagy induction can enhance clearance of toxic intracellular waste associated with neurodegenerative diseases and has been comprehensively demonstrated to improve lifespan in yeast, worms, flies, rodents and primates. The situation, however, has been complicated by the identification that autophagy up-regulation can also occur during ageing. Indeed, in certain situations, reduced autophagosome induction may actually provide benefits to ageing cells. Future studies will undoubtedly improve our understanding of exactly how the multiple signals that are integrated to control appropriate autophagy activity change during ageing, what affect this has on autophagy and to what extent autophagy contributes to age-associated pathologies. Identification of mechanisms that influence a healthy lifespan is of economic, medical and social importance in our ‘ageing’ world.

Kaposis sarcoma and diabetes mellitus

1971 ◽  
Vol 104 (4) ◽  
pp. 442-444 ◽  
Author(s):  
R. Tankel
Keyword(s):  
Diabetes Mellitus
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