E. King

ORCID: 0000-0002-4950-5662
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About
Contact & Profiles
Research Areas
  • Adipose Tissue and Metabolism
  • Peroxisome Proliferator-Activated Receptors
  • Mitochondrial Function and Pathology
  • Metabolism, Diabetes, and Cancer
  • Metabolism and Genetic Disorders
  • Redox biology and oxidative stress
  • Eicosanoids and Hypertension Pharmacology
  • Muscle metabolism and nutrition
  • Autophagy in Disease and Therapy
  • Renin-Angiotensin System Studies
  • Epigenetics and DNA Methylation
  • Adenosine and Purinergic Signaling
  • Protein Degradation and Inhibitors
  • Sirtuins and Resveratrol in Medicine
  • Natural Antidiabetic Agents Studies
  • Diabetes Treatment and Management
  • Infective Endocarditis Diagnosis and Management
  • Nutrition and Health in Aging
  • Angiogenesis and VEGF in Cancer
  • Muscle Physiology and Disorders
  • Nitric Oxide and Endothelin Effects
  • Otolaryngology and Infectious Diseases
  • Liver Disease Diagnosis and Treatment
  • Kruppel-like factors research
  • Pancreatic function and diabetes

Baker Heart and Diabetes Institute
2018-2025

Monash University
2018-2025

Marshall University
2025

The Heart Research Institute
2015-2019

St Bartholomew's Hospital
1972

Huddersfield Royal Infirmary
1972

St. Leonards Hospital
1972

During mitochondrial damage, information is relayed between the mitochondria and nucleus to coordinate precise responses preserve cellular health. One such pathway integrated stress response (mtISR), which known be activated by DNA (mtDNA) damage. However, causal molecular signals responsible for activation of mtISR remain mostly unknown. A gene often associated with mtDNA mutations/deletions Polg1, encodes Polymerase γ (PolG). Here, we describe an inducible, tissue specific model PolG...

10.1038/s41467-025-57299-3 article EN cc-by-nc-nd Nature Communications 2025-03-08

Here, we present a case of infective endocarditis (IE) caused by Gemella sanguinis, pathogen that rarely causes human infection. The patient in this was an otherwise healthy 50-year-old man who presented with gradually worsening shortness breath, weight loss, fatigue, chills, and leg swelling for six weeks. He had no prior history cardiac disease never used intravenous drugs, but he undergone extensive dental work following military-associated injury. A workup IE done, echocardiography...

10.7759/cureus.78837 article EN Cureus 2025-02-11

10.1152/ajplegacy.1967.212.1.179 article EN American Journal of Physiology-Legacy Content 1967-01-01

The effective storage of lipids in white adipose tissue (WAT) critically impacts whole body energy homeostasis. Many genes have been implicated WAT lipid metabolism, including tripartite motif containing 28 (Trim28), a gene proposed to primarily influence adiposity via epigenetic mechanisms embryonic development. However, the current study we demonstrate that mice with deletion Trim28 specifically committed adipocytes, also develop obesity similar global models, highlighting...

10.1038/s41467-020-20434-3 article EN cc-by Nature Communications 2021-01-04

In patients with portal hypertension, plasma insulin levels were raised both fasting and after oral glucose or intravenous tolbutamide. This supports previous suggestions that resistance to endogenous plays a major role in producing the impaired tolerance found chronic hepatic dysfunction. The operation of portacaval anastomosis was followed by fructose tolerance, but did not significantly change tolerance. Plasma unchanged operation, either following stimulus an load response only higher...

10.1136/gut.13.1.58 article EN Gut 1972-01-01

Fenofibrate, a peroxisome proliferator-activated receptor α (PPARα) agonist, reduces lower limb amputations in patients with type 2 diabetes. The mechanism is, however, unknown. In this study, we demonstrate that fenofibrate markedly attenuates diabetes-related impairment of ischemia-mediated angiogenesis. murine model hindlimb ischemia, daily oral treatment restored diabetes-impaired blood flow recovery, foot movement, capillary density, vessel diameter, and vascular endothelial growth...

10.2337/db17-0926 article EN Diabetes 2019-02-14

Aims The induction of heat shock protein 72 (Hsp72) via heating, genetic manipulation or pharmacological activation is metabolically protective in the setting obesity‐induced insulin resistance across mammalian species. In this study, we set out to determine whether overexpression Hsp72, specifically skeletal muscle, can protect against high‐fat diet (HFD)‐induced obesity and resistance. Materials methods An Adeno‐Associated Viral vector (AAV), designed overexpress Hsp72 muscle only, was...

10.1111/dom.13319 article EN Diabetes Obesity and Metabolism 2018-04-13

Type 2 diabetes mellitus (T2DM), a condition characterised by insulin resistance (IR) and skeletal muscle mitochondrial abnormalities, is leading cause of death in developed societies. Much work has postulated that improving pathways linked to health, including autophagy, may be potential avenue prevent or treat T2DM. Given the recent data indicating role for tripartite motif-containing 28 (TRIM28) autophagy pathways, we investigated whether muscle-specific deletion TRIM28 might impact on...

10.1530/joe-23-0210 article EN Journal of Endocrinology 2023-09-19

ABSTRACT During mitochondrial damage, information is relayed between the mitochondria and nucleus to coordinate precise responses preserve cellular health. One such pathway integrated stress response (mtISR), which specifically activated by DNA (mtDNA) damage. However, causal molecular signals responsible for this activation remain elusive. A gene often associated with mtDNA mutations/deletions Polg1 , encodes Polymerase γ (PolG). Here, we describe what our knowledge first conditional muscle...

10.1101/2024.06.02.597064 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2024-06-03

Phenethylbiguanide (DBI) has been used for its hypoglycemic action in the treatment of diabetes mellitus 206 patients a period two years. Adequacy management, maintained 128 patients, was judged by absence diabetic symptoms and drug's side-effects (nausea, anorexia, gastrointestinal disturbances). DBI made exogenous insulin unnecessary 110 who were known to have partial supply from their pancreas. The requirement decreased one-half when 18 produced no natural given DBI. Severe intolerance...

10.1097/00043764-196008000-00046 article EN Journal of Occupational and Environmental Medicine 1960-08-01
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