Marlon E. Cerf

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Beta cell dysfunction and insulin resistance are inherently complex with their interrelation for triggering the pathogenesis of diabetes also somewhat undefined. Both pathogenic states induce hyperglycemia and therefore increase insulin demand. Beta cell dysfunction results from inadequate glucose sensing to stimulate insulin secretion therefore elevated(More)
Type 2 diabetes is primarily associated with insulin resistance and beta-cell dysfunction. Maintenance of functional mature beta-cells is imperative for ensuring glucose homeostasis. This can be achieved by optimal expression of key transcription factors that are required for normal pancreatic development and maintaining beta-cell function. Defining the(More)
The pancreas is characterized by a major component, an exocrine and ductal system involved in digestion, and a minor component, the endocrine islets represented by islet micro-organs that tightly regulate glucose homoeostasis. Pancreatic organogenesis is strictly co-ordinated by transcription factors that are expressed sequentially to yield functional(More)
Plasma kallikrein (PK) is a cofactor in blood coagulation and modulates inflammation through the release of bradykinin. Previously it was believed that plasma prekallikrein (PPK), the precursor of PK and a member of the serine protease superfamily, was synthesized exclusively by hepatocytes and secreted into circulation. However, recent studies show that(More)
Hyperglycemia and compromised beta-cell development were demonstrated in neonatal rats programmed with a gestational high-fat diet. The aim of this study was to determine whether these changes were attributed to impaired insulin release and altered immunoreactivity of Pdx-1, glucokinase (GK), and glucose transporter (GLUT)-2 in high-fat-programmed neonates.(More)
High-fat programming, by exposure to a high-saturated-fat diet in utero and/or during lactation, compromises beta-cell development and function in neonatal and weanling offspring. Therefore, high-fat programming effects were investigated on metabolism and islet architecture in young adult rats. Three-month-old male and female Wistar rat offspring were(More)
High saturated fat intake contributes to insulin resistance, beta-cell failure, and type 2 diabetes. Developmental programming refers to a stimulus or insult during critical periods of life which includes fetal and subsequent early neonatal life. Programming alters offspring physiology and metabolism with both immediate and lasting consequences. Maternal(More)
High-fat feeding reduces the expression of GLUT-2 and the glycolytic enzyme glucokinase (GK). The transcription factor, pancreatic duodenal homeobox-1 (Pdx-1), is important for beta-cell maintenance. The aim of the present study was to determine, in weanling Wistar rats, the effect of a maternal high-fat diet (HFD) during defined periods of gestation and(More)
Diabetic nephropathy is a complex disease that involves increased production of free radicals which is a strong stimulus for the release of pro-inflammatory factors. We evaluated the renal protective effect of kolaviron (KV) - a Garcinia kola seed extract containing a mixture of 5 flavonoids, in diabetes-induced nephrotoxic rats. Male Wistar rats were(More)
Type 2 diabetes is primarily associated with beta-cell failure, insulin resistance and elevated hepatic glucose production. The islet beta-cell is specialized for the synthesis, storage and secretion of insulin. Beta-cell failure is characterized by the inability of the beta-cell to secrete sufficient insulin in response to glucose, which ultimately results(More)