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Articles 1 - 7 of 7
Full-Text Articles in Endocrinology
The Role Of Inflammatory Cytokines In The Bidirectional Relationship Between Periodontitis And Diabetes Mellitus, Andrew R. Witty
The Role Of Inflammatory Cytokines In The Bidirectional Relationship Between Periodontitis And Diabetes Mellitus, Andrew R. Witty
Oral Health
Periodontitis and type 2 diabetes mellitus are associated with each other in a bidirectional relationship. The mechanism by which diabetes affects periodontitis is understood to be due to the inflammatory effects of hyperglycemia (high blood glucose levels) and a hospitable environment for sugar-consuming bacteria. Periodontitis is known to be associated with higher levels of glycated hemoglobin (HbA1c), a long-term measurement of blood glucose control, and treatment of periodontitis reduces HbA1c. Inflammation caused by periodontitis induces insulin resistance (which leads to higher blood glucose levels), but due to the complex nature of inflammation it is difficult to …
Regulated Translocation Of Neutral Sphingomyelinase-2 To The Plasma Membrane Drives Insulin Resistance In Steatotic Hepatocytes, Salim S. El-Amouri, Alexander A. Karakashian, Erhard Bieberich, Mariana N. Nikolova‑Karakashian
Regulated Translocation Of Neutral Sphingomyelinase-2 To The Plasma Membrane Drives Insulin Resistance In Steatotic Hepatocytes, Salim S. El-Amouri, Alexander A. Karakashian, Erhard Bieberich, Mariana N. Nikolova‑Karakashian
Markey Cancer Center Faculty Publications
Abstract Obesity-associated diabetes is linked to the accumulation of ceramide in various organs, including the liver. The exact mechanisms by which ceramide contributes to diabetic pathology are unclear, but one proposed scenario is that ceramide accumulation may inhibit insulin signaling pathways. It is unknown however whether the excess ceramide is generated proximal to the insulin receptor, that is, at the plasma membrane (PM), where it could affect the insulin signaling pathway directly, or the onset of insulin resistance is due to ceramide- induced mitochondrial dysfunction and/or lipotoxicity. Using hepatic cell lines and primary cultures, gain- and loss- of function approach, …
Gpr75 Deficiency Attenuates High Fat Diet-Driven Obesity And Glucose Intolerance, Sakib Hossain
Gpr75 Deficiency Attenuates High Fat Diet-Driven Obesity And Glucose Intolerance, Sakib Hossain
NYMC Student Theses and Dissertations
Recently, a collaboration between Regeneron Pharmaceuticals and the Schwartzman-Garcia labs at New York Medical College published an exome sequencing study of individuals across the United Kingdom, United States, and Mexico which concluded that individuals possessing non-functioning, truncated mutations to the orphan g protein coupled receptor (GPCR), GPR75, had lower BMI and 54% reduced likelihood of obesity. The present study was undertaken to fully characterize the metabolic phenotype of Gpr75 deficient mice when fed a high fat diet (HFD) and explore potential mechanisms by which GPR75 activation links to increased adiposity and decreased glucose tolerance. After 14 weeks of HFD-feeding we …
Modulation Of Glucose Homeostasis By Nucleotide P2y2 Receptor And Biological Sex, Hailee Anne Marino
Modulation Of Glucose Homeostasis By Nucleotide P2y2 Receptor And Biological Sex, Hailee Anne Marino
Graduate Theses/Dissertations
Recent insights into the pathological role of Nucleotide P2Y2 receptor suggest P2Y2R involvement in high fat diet-induced obesity and potentiates insulin resistance. However, these recent insights do not demonstrate how P2Y2R modulates glucose homeostasis under physiological conditions. Further, it remains unknown how sex biological factors influence P2Y2R receptor signaling in the regulation of glucose homeostasis. The research objective for the present study is to elucidate the novel roles of P2Y2 in fasting blood glucose and glucose tolerance (basal insulin sensitivity) under resting conditions in males and females. We expected that under physiological …
Novel Mitochondrial Complex I Inhibitors Restore Glucose-Handling Abilities Of High-Fat Fed Mice, Darren Martin, Siobhan Leonard, Robert Devine, Clara Redondo, Gemma Kinsella, Conor Breen, Victoria Mceneaney, Mary Rooney, Tim Munsey, Richard Porter, Asipu Sivaprasadarao, John Stephens, John Findlay
Novel Mitochondrial Complex I Inhibitors Restore Glucose-Handling Abilities Of High-Fat Fed Mice, Darren Martin, Siobhan Leonard, Robert Devine, Clara Redondo, Gemma Kinsella, Conor Breen, Victoria Mceneaney, Mary Rooney, Tim Munsey, Richard Porter, Asipu Sivaprasadarao, John Stephens, John Findlay
Articles
Metformin is the main drug of choice for treating type 2 diabetes, yet the therapeutic regimens and side effects of the compound are all undesirable and can lead to reduced compliance. The aim of this study was to elucidate the mechanism of action of two novel compounds which improved glucose handling and weight gain in mice on a high-fat diet. Wildtype C57Bl/6 male mice were fed on a high-fat diet and treated with novel, anti-diabetic compounds. Both compounds restored the glucose handling ability of these mice. At a cellular level, these compounds achieve this by inhibiting complex I activity in …
The Effect Of Run Sprint Interval Training On Diabetic Metabolic Markers In Prediabetic Adults, Kathryn L. Hilovsky
The Effect Of Run Sprint Interval Training On Diabetic Metabolic Markers In Prediabetic Adults, Kathryn L. Hilovsky
Masters Theses, 2010-2019
Abstract
Purpose: The primary purpose of this study was to compare the effects of an 8-week run-sprint interval training (R-SIT) and continuous moderate-intensity training (MIT) on fasting blood glucose, HbA1c, insulin sensitivity, and β-cell function in sedentary, prediabetic adults. Secondary outcomes of the study included anthropometric, body composition variables, and aerobic capacity.
Methods: Sedentary, physician diagnosed prediabetic individuals were randomized into R-SIT (n=7, BMI 36.76 ± 9.79) or MIT (n=8, BMI 40.59 ± 12.49) interventions. Subjects participated in supervised exercise three times a week and attended a Diabetes Prevention Program course, once weekly. R-SIT participants performed 4-6 x 30-second …
Linking Environmental Toxicant Exposure To Diabetes Susceptibility, Jannifer Beth Tyrrell
Linking Environmental Toxicant Exposure To Diabetes Susceptibility, Jannifer Beth Tyrrell
Wayne State University Dissertations
An important and unresolved question in the environmental health field is whether exposure to common environmental toxicants, such as dioxin and heavy metals like Pb, increase the risk of developing diabetes, especially in combination with other common metabolic stressors such as obesity.
Previous studies suggested that dioxin exposure increased peripheral insulin resistance but did not appear to cause fasting hyperglycemia or elevated hepatic glucose output. In concordance with those findings we observed that dioxin treatment caused a strong suppression of the expression of the key hepatic gluconeogenic genes PEPCK and G6Pase. However, this suppression was not solely mediated by the …