A5060212009- Pancreatic function and diabetes
- Diabetes Treatment and Management
- Diabetes and associated disorders
- Metabolism, Diabetes, and Cancer
- Adipose Tissue and Metabolism
- Diet and metabolism studies
- Receptor Mechanisms and Signaling
- Metabolism and Genetic Disorders
- Inflammatory mediators and NSAID effects
- Hormonal and reproductive studies
- Adrenal Hormones and Disorders
- Thyroid Disorders and Treatments
- Amino Acid Enzymes and Metabolism
- Acute Lymphoblastic Leukemia research
- Connective tissue disorders research
- Bone health and treatments
- Neurological and metabolic disorders
- Pancreatitis Pathology and Treatment
- Growth Hormone and Insulin-like Growth Factors
- Biomedical Research and Pathophysiology
- Gut microbiota and health
- Dietary Effects on Health
- Peroxisome Proliferator-Activated Receptors
- Myasthenia Gravis and Thymoma
- Neurological Disorders and Treatments
William S. Middleton Memorial Veterans Hospital
2019-2024
University of Wisconsin–Madison
2016-2024
Vanderbilt University Medical Center
2023
Nashville Oncology Associates
2021
Madison Group (United States)
2017
München Klinik
1938-1941
Schmerzklinik Kiel
1932-1935
The transition from β-cell compensation to failure is not well understood. Previous works by our group and others have demonstrated a role for Prostaglandin EP3 receptor (EP3), encoded the Ptger3 gene, in loss of functional mass Type 2 diabetes (T2D). primary endogenous ligand arachidonic acid metabolite prostaglandin E2 (PGE2). Expression pancreatic islet PGE2 synthetic enzymes and/or excretion itself all been shown be upregulated mouse human islets isolated animals or organ donors with...
The inhibitory G protein alpha-subunit (Gαz) is an important modulator of beta-cell function. Full-body Gαz-null mice are protected from hyperglycemia and glucose intolerance after long-term high-fat diet (HFD) feeding. In this study, at a time point in the feeding regimen where WT only mildly intolerant, transcriptomics analyses reveal islets HFD-fed Gαz KO have dramatically altered gene expression pattern as compared with mice, entire pathways not being more strongly upregulated or...
Elevated islet production of prostaglandin E2 (PGE2), an arachidonic acid metabolite, and expression receptor subtype EP3 (EP3) are well-known contributors to the β-cell dysfunction type 2 diabetes (T2D). Yet, many same pathophysiological conditions exist in obesity, little is known about how PGE2 signaling pathway influences nondiabetic function. In this work, plasma metabolite levels were quantified a cohort T2D human subjects identify their relationship with glycemic control, systemic...
1. Bei gesunden Tieren steigt Milchsaure und Blutzucker nach Adrenalininjektion regelmasig recht erheblich an. 2. Bei Schadigungen verschiedener Art (Urethan, Sufrogel, Hunger, Thyroxin u. a.), durch die eine akute Kreatinurie hervorgerufen wird, fehlt Milchsaureerhohung Adrenalin. 3. Wird hervorgerufen, sich uber langere Zeit erstreckt, ist wieder vorhanden, auch wenn noch grosere Mengen von Kreatin ausgeschieden werden.
Islet prostaglandin EP3 receptor (EP3) signaling is well known as upregulated in the pathophysiological conditions of type 2 diabetes, contributing to β-cell dysfunction. Unexpected findings mouse models non-obese insulin sensitivity and resistance provide a new dimension our understanding key modulator secretion. A previously unknown relationship between penetrance rat promoter-driven germline floxed allele recombination critical consider when creating β-cell-specific knockouts.
Abstract Disclosure: J.E. Stanley: None. A. Reuter: K. Sellick: A.D. Attie: M.P. Keller: E. Dean: Glucagon secreted from pancreatic islet α cells stimulates both hepatic glycogenolysis and gluconeogenesis resulting in the fractional extraction of amino acids blood. Thus, glucagon glucose output raises blood glucose. When liver signaling is impaired, acid accumulation (hyperaminoacidemia) promotes subsequent cell hyperplasia hyperglucagonemia via this liver-α-cell axis, an endocrine feedback...
Signaling through prostaglandin E
Abstract Objective Signaling through Prostaglandin E3 Receptor (EP3), a G protein-coupled receptor for E series prostaglandins such as prostaglandin 2 (PGE ), has been linked to the beta-cell dysfunction and loss of mass in type diabetes (T2D). In beta-cell, EP3 is specifically coupled unique cAMP-inhibitory protein, z . Divergent effects agonists antagonists or Gα on function, replication, survival depending whether islets are isolated from mice humans lean healthy, 1 diabetic, T2D state...
Abstract When homozygous for the Leptin Ob mutation (Ob), Black-and-Tan Brachyury (BTBR) mice become morbidly obese and severely insulin resistant, by 10 weeks of age, frankly diabetic. Previous work has shown Prostaglandin EP3 Receptor (EP3) expression activity is up-regulated in islets from BTBR-Ob as compared to lean controls, actively contributing their beta-cell dysfunction. In this work, we aimed test impact beta-cell-specific loss on phenotype crossing Ptger3 floxed with Rat promoter...
Drug Prescribing for Patients with Chronic Kidney Disease in General Practice: a Cross-Sectional Study
It has recently been established that changes in the gut microbiotic profile are influential development of obesity and type 2 diabetes mellitus (T2DM). Homozygosity for leptin Ob mutation BTBR mouse strain induces hyperphagia resulting obesity, insulin resistance, ultimately severe T2DM with full penetrance by 10 weeks age. The ob/ob is a strong, well‐accepted pre‐clinical model T2DM: no one ever reported conditions which mice do not become diabetic. We found housed specific “dirty”...
Mortality from cardiovascular disease has declined over the past couple of decades, while diabetic population, with nearly two‐fold greater risk, seen minimal benefit. A significant contributing factor to pro‐thrombotic state is downregulation anti‐platelet activating mechanisms that normally maintain high levels inhibitory cAMP prevent aggregation. Yet these same signaling pathways are important proper platelet function may also be in insulin‐secreting beta‐cell, as by pancreatic beta cells...