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insulinoma/triglyceride
Linkki tallennetaan leikepöydälle
Sivu 1 alkaen 34 tuloksia
Fatty acid and glucose incorporation into human adipose tissue in non-insulin-dependent diabetes and in insulinoma. Inverse relations with plasma triglyceride and glucose concentrations.
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Decreased fatty acid and glucose incorporation into human adipose tissue (FIAT and GLIAT) are frequently found in primary hypertriglyceridemia (HTG) and might also contribute to the defective removal of lipoprotein triglyceride (TG) in non-insulin-dependent diabetes mellitus (NIDDM). To study this
Reduction of visceral adiposity after operation in a subject with insulinoma.
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Generally, it is considered that visceral fat brings insulin resistance and hyper-insulinemia, in the mechanisms of metabolic syndromes. However, whether hyperinsulinemia brings about accumulation of visceral fat is not clear. We followed a case of insulinoma that caused primary hyperinsulinemia,
The lipid-chemical features of the metastatic tissues into the liver from the human gastric cancer, large intestinal cancer and malignant insulinoma.
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In order to clarify the biochemical features of metastatic tissues into the liver of human cancerous cells, 12 of primary cancerous tissues and 3 of metastatic tissues of the large intestinal cancer, 6 of primary cancerous tissues and 2 of metastatic tissues of the gastric cancer, and 3 of primary
Associations of ATP-binding cassette transporter A1 and G1 with insulin secretion in human insulinomas.
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OBJECTIVE
Adenosine triphosphate-binding cassette transporter A1 (ABCA1) and G1 (ABCG1) are 2 important cholesterol transporters in human pancreatic β-cells. The aim of this study was to investigate their alteration in insulinomas and their potential associations with abnormal insulin secretion in
Biochemical differences between human malignant and benign insulinoma tissues.
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Five cases of malignant insulinoma and 2 cases of benign insulinoma were studied lipid-chemically. Tissues were collected by surgical operation or biopsy under peritoneoscopy. The total lipid was extracted from each tissue, and one part of each total lipid was separated into phospholipid,
Effects of diet-induced ketosis in rats with hypoglycaemia due to a serially transplantable insulinoma.
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In view of the ability of ketones to partially replace glucose as an alternative fuel in the brain, the potential protective effects of diet-induced ketosis were examined in male NEDH rats with hypoglycaemia due to a serially transplantable radiation-induced insulinoma. Ketosis was induced by daily
Effect of endogenous organic hyperinsulinaemia on blood pressure and serum triglycerides.
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Hyperinsulinaemia and insulin resistance have been hypothesized to be the common pathophysiological factor of hypertension, NIDDM and obesity. To evaluate the possible role of hyperinsulinaemia and insulin resistance on hypertension, we studied a group of 37 patients with insulinoma who were
Absence of clinically overt atherosclerotic vascular disease and adverse changes in cardiovascular risk factors in 70 patients with insulinoma.
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Hyperinsulinemia has been assumed to contribute to the pathogenesis of atherosclerosis. To assess the reliability of such claim we planned a retrospective study on a cohort of patients with pancreatic insulin producing neoplasm. A correlation was sought between fasting insulin plasma levels and the
Focal hepatic steatosis surrounding a metastatic insulinoma.
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Reported herein is a case of focal hepatic steatosis surrounding a metastatic insulinoma in the liver of a 69-year-old woman. The patient complained of losing consciousness after meals, and hypoglycemia and hyperinsulinemia were confirmed. On CT and abdominal angiography a mass, 1 cm in diameter,
Hypertension and dyslipidemia in patients with insulinoma.
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Hyperinsulinemia is alleged to contribute to the pathogenesis of hypertension and dyslipidemia (hypertriglyceridemia) in the setting of insulin resistance. To assess the association among hyperinsulinemia, hypertension, and hypertriglyceridemia in the absence of insulin resistance, we determined
A case of insulinoma with non-alcoholic fatty liver disease: Roles of hyperphagia and hyperinsulinemia in pathogenesis of the disease.
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Nonalcoholic fatty liver disease (NAFLD) is a serious health-related condition all over the world; the number of patients is increasing in Asian countries including Japan. Better understanding of its pathophysiology is required to develop effective therapeutics, as patients may go on to develop
PPARalpha suppresses insulin secretion and induces UCP2 in insulinoma cells.
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Fatty acids may promote type 2 diabetes by altering insulin secretion from pancreatic beta cells, a process known as lipotoxicity. The underlying mechanisms are poorly understood. To test the hypothesis that peroxisome proliferator-activated receptor alpha (PPARalpha) has a direct effect on islet
AMP-activated protein kinase agonist dose dependently improves function and reduces apoptosis in glucotoxic beta-cells without changing triglyceride levels.
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Prolonged hyperglycaemia leads to impaired glucose-stimulated insulin secretion (GSIS) and apoptosis in insulin-producing beta-cells. The detrimental effects have been connected with glucose-induced lipid accumulation in the beta-cell. AMP-activated protein kinase (AMPK) agonist,
Knockdown of pyruvate carboxylase or fatty acid synthase lowers numerous lipids and glucose-stimulated insulin release in insulinoma cells.
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We previously showed that knockdown of the anaplerotic enzyme pyruvate carboxylase in the INS-1 832/13 insulinoma cell line inhibited glucose-stimulated insulin release and glucose carbon incorporation into lipids. We now show that knockdown of fatty acid synthase (FAS) mRNA and protein also
RNA-binding protein HuD reduces triglyceride production in pancreatic β cells by enhancing the expression of insulin-induced gene 1.
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Although triglyceride (TG) accumulation in the pancreas leads to β-cell dysfunction and raises the chance to develop metabolic disorders such as type 2 diabetes (T2DM), the molecular mechanisms whereby intracellular TG levels are regulated in pancreatic β cells have not been fully elucidated. Here,
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