Ghrelin and leptin are the hormones that influence endocrine and exocrine functions of the pancreas and regulate feeding behaviors and energy metabolism. The aim of this study was to investigate the levels of ghrelin and leptin in pancreatitis of different severities and the relation of these hormones with blood glucose level and proinflammatory cytokines. The study was performed on 90 Wistar Albino rats. Three experimental groups composed of 30 rats were established: control group, 0.9% NaCl solution was injected intraperitoneally (i.p); acute edematous pancreatitis (AEP) group, 1 microg/100 g cerulein was injected i.p. five times, at 1-hr intervals; and acute necrotizing pancreatitis (ANP) group, 500 mg/100 g L-arginine was injected i.p. Ten animals in each group were sacrificed under anesthesia 12, 24 and 48 hr after the last injection. After blood withdrawal, the pancreas was totally excised. The levels of blood sugar, lipase, serum tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), ghrelin, and leptin were investigated and histopathologic examination was performed. Following pancreatitis induction, serum ghrelin levels increased at 24 hr and reached the peak level at 48 hr. Its level in the AEP group was higher than in the ANP group. Serum leptin levels in the AEP and ANP groups increased after 12 hr and stayed at high levels until 48 hr compared with the control group. Similarly to ghrelin and leptin, blood glucose levels increased in both pancreatitis groups, but the increase was more prominent in the ANP group, with levels >200 mg/ml at 48 hr. The levels of TNF-alpha and IL-1beta in the AEP and ANP groups reached the peak level at 24 hr and then decreased to a level close to that of the control group at 48 hr. We conclude that serum leptin and ghrelin levels increase in the first 48 hr of AEP and ANP. As the serum ghrelin levels in ANP are higher than in AEP, it can be used as a marker to show the severity of pancreatitis. While TNF-alpha and IL-1beta can be used as a prognostic factor in the first 24 hr, ghrelin and leptin can be used subsequently.
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http://dx.doi.org/10.1007/s10620-006-9150-0 | DOI Listing |
J Clin Med
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Clinical Department of Gynecologic Surgery and Oncology, Wroclaw Medical University, Borowska 213, 50-556 Wroclaw, Poland.
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View Article and Find Full Text PDFMedicina (Kaunas)
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Department of Human Sciences and Promotion of the Quality of Life, San Raffaele Rome Open University, 00166 Rome, Italy.
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View Article and Find Full Text PDFAnimals (Basel)
December 2024
Department of Animal Science, State University of Maringá (UEM), Maringá 87020-900, Brazil.
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Mother Infant Research Institute at Tufts Medical Center, Boston, MA, United States.
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J Lipid Res
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Department of Endocrinology and Metabolism, Shunde Hospital of Southern Medical University (The First People's Hospital of Shunde Foshan), Foshan, Guangdong Province, China. Electronic address:
High-fat diet (HFD) -induced microglial activation contributes to hypothalamic inflammation and obesity, but the mechanisms linking microglia to structural changes remain unclear. This study explored the role of microglia in impairing hypothalamic synaptic plasticity in diet-induced obesity (DIO) mice and evaluated the therapeutic potential of semaglutide (Sema) and minocycline (MI). Six-week-old C57BL/6J mice were divided into low-fat diet (LFD) and HFD groups.
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