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Selenium is an essential trace element in the diet of mammals which is important for many physiological functions.
Feedback regulation between hepatic Sepp1 and pancreatic insulin under the normal insulin-sensitive condition.
AcknowledgmentsThis work was supported by National Nature Science Foundation of China (Grant number: 81200571). Digestive enzymes (proteases, lipases and amylases) are substances that divide the food absorbed in the small to small particles. The different possibilities of examinations and other diagnostic measures are addressed in a discussion between doctor and patient. Endoscopic retrograde cholangiopancreatography (ERCP): a review essential to visualize the bile duct and main pancreatic duct. If the cancer is confined only to the pancreas, it can sometimes be resected completely by surgery. The pancreas is resected in part or in whole, to do this, the surgeon makes an incision in the middle of the abdomen. For major surgery, operative mortality is high (3%) and adverse effects are observed in 30-50% of cases.
Thus, the patient should take digestive enzyme supplements with each meal and blood sugar should be controlled by insulin injections. Copyright © 2012 Rayur, All trademarks are the property of the respective trademark owners. Schematic diagram depicting activation of proteolytic enzymes, possibly through colocalization of zymogen granules and lysosomes, and subsequent rupture of zymogen granules releasing the activated enzymes into the cytoplasm of the pancreatic acinar cell. From the 2010 revision of the Complete Home Medical Guide © Dorling Kindersley Limited. The subjects, conditions and treatments covered in this encyclopaedia are for information only and may not be covered by your insurance product should you make a claim. However, a number of epidemiological studies have suggested that high selenium status is a possible risk factor for the development of type 2 diabetes, although they cannot distinguish between cause and effect. Circulating high glucose concentration stimulates the expression of insulin in the pancreas and Sepp1 in the liver.
Sepp1 and Energy MetabolismObesity is closely related to insulin resistance and is a strong risk factor in the development of type 2 diabetes. The disease affects mainly men between 60 and 80 years and is more common in men than in women. It is in the middle of the upper abdominal cavity, just up the kidneys, and fits into the curve of the duodenum, behind the stomach. If pancreatic function is impaired, digestion and glucose metabolism are severely disrupted.
To do this, an endoscopy of the stomach and small intestine is performed through an endoscope mobile. The procedure is the same for ablations of parts of the stomach, small intestine or the biliary system.
In addition, the patient will be exposed to risks inherent in any surgery, that is to say, delays wound healing, bleeding, thrombosis, wound infections, fever and allergic reactions to certain medications or bandages.
Despite this treatment, the absorption of nutrients will be disrupted and patients often suffer from impaired gastric emptying and intestinal disorders. The activated enzymes then undergo disordered basolateral discharge from the acinar cell into the pancreatic parenchyma.
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It plays a major role in digestion, releasing enzymes that break down fat, starch, and proteins through the pancreatic ducts into the intestine.
Selenoprotein P (Sepp1) is central to selenium homeostasis and widely expressed in the organism.
While its importance for the brain [1], fertility [2], immune [3] and thyroid functions [4] and cancer prevention [5] is well established, the association between selenium and glucose metabolism is conflicting. If the increasing Sepp1 is transported into the pancreas and collaterally enhances insulin production, then sufficient insulin may feedback to inhibit hepatic Sepp1 production.


Weight changes have also been observed in several mouse strains with Sepp1-associated gene knockout. In recent years, there is nevertheless an increase of pancreatic cancer among younger patients. The pancreas consists of endocrine part that secretes hormones (insulin, glucagon) and exocrine part, which produces pancreatic enzymes (digestive enzymes). The orifice of the bile duct and main pancreatic duct (papilla), located in the small intestine, is full of contrast through a catheter. If total removal of the pancreas, the patient can no longer produce or digestive enzymes or insulin. It also contains clusters of cells, called islets of Langerhans, that secrete hormones directly into the bloodstream. Here we review the interaction between Sepp1 and glucose metabolism with an emphasis on experimental evidence.
Despite the expectation that selenium might prevent the development of diabetes owing to its antioxidant and insulin-mimetic properties [6,7,8], in recent years, some epidemiological studies, including cross-sectional studies and longitudinal studies, have shown that supranutritional selenium intake or high plasma selenium levels are a possible risk factor for the development of type 2 diabetes or metabolic syndrome [9,10,11,12]. X-rays are then practiced; they allow you to view channels, and any interruptions and obstacles to the flow. In models with or without gene modification, glucose and insulin can regulate Sepp1 expression in the pancreas and liver, and vice versa. However, there are also studies that support a decreased risk of type 2 diabetes at higher levels of Se intake [13,14,15]. When mice were fed a high-fat, high-sucrose diet, Sepp1 knockouts tended to have more body-weight gain, but daily food intake and basal energy expenditure significantly increased and adipocyte hypertrophy attenuated, compared to wild-type mice [42]. In the prospective observational Epidemiology of Vascular Ageing (EVA) study, 1162 participants with complete data were analyzed and it was found that high plasma selenium correlated with a decreased risk of onset of hyperglycaemia during a 9-year follow-up period in elderly men (though not in women) [14].
Combining these data suggests that there could be a feedback regulation between hepatic Sepp1 and pancreatic insulin and that increasing circulating Sepp1 might be the result rather than the cause of abnormal glucose metabolism. However, most randomized controlled trials showed that selenium supplementation had no protective or adverse effect for type 2 diabetes [16,17,18], except the Nutritional Prevention of Cancer (NPC) Trial. Future studies specifically designed to overexpress Sepp1 are needed in order to provide a more robust link between Sepp1 and type 2 diabetes. Recently, a connection between metabolic energy regulation and selenium metabolism through selenocysteinelyase (Scly), which mediates the pathway for recycling selenium, was reported [54]. Both Yang and Misu reported that circulating SEPP1 levels were associated with dysregulation of glucose metabolism in humans [21,22].
Scly is the enzyme that supplies selenium for selenoprotein biosynthesis via decomposition of the amino acid Sec [55,56].
In the Korean study, serum SEPP1 levels were significantly higher in patients with type 2 diabetes (n = 40) or prediabetes (n = 40) than in those with normal glucose tolerance (n = 20) [21].
At the same time, Sepp1 mRNA was obviously upregulated in the liver but the protein level in the circulation remained unchanged.
Furthermore, upon dietary selenium restriction, Scly knockout mice developed several characteristics of the metabolic syndrome, such as fatty liver and hypercholesterolemia, with aggravated hyperleptinemia, hyperinsulinemia, and glucose intolerance [54]. Sepp1 mRNA was upregulated but the protein level did not change in the liver, and circulating Sepp1 significantly decreased compared with the control [54]. Here, we review the interaction between Sepp1 and glucose metabolism with the emphasis on experimental evidence which could underlie the cause-and-effect relationship of selenium and glucose metabolism.
These studies illustrate that Sepp1 could be involved in energy metabolism, which suggests that the relationship between Sepp1 and glucose metabolism should be explored. Moreover, with the development of animal models with genetic alterations, there are wider opportunities to elucidate the mechanisms under different conditions.
The role of selenium in inflammation and immunity: From molecular mechanisms to therapeutic opportunities.
Metabolic effect of sodium selenite: Insulin-like inhibition of glucagon-stimulated glycogenolysis in the isolated perfused rat liver.
Steinbrenner and colleagues also observed that selenium compounds at 1 ?M can significantly upregulate Sepp1 gene expression in INS-1 cells cultured under normoglycemic conditions (5 mM glucose) [32]. It could be speculated that selenium may stimulate insulin production mediated by increasing Sepp1 expression in pancreatic ? cells.


However, high glucose concentrations dose-dependently suppressed the selenium-induced elevation of Sepp1 mRNA level, by inhibiting Sepp1 promoter activity. On the other hand, it is observed that high glucose concentrations (11 or 22 mM), without treatment with extra selenium compounds, significantly down-regulated Sepp1 expression by more than 70% in primary islets isolated from mouse pancreas, when compared to 5.5 mM glucose. In contrast to the situation in the pancreas, gene expression and secretion of Sepp1 is increased at high glucose concentrations in rat H4IIEC hepatocytes and rat primary hepatocytes [41,42], while treatment with the antidiabetic drug metformin attenuated Sepp1 mRNA expression and secretion, although the applied dose of metformin was far higher than the therapeutic level in humans [41]. That suggests that the rising secretion of insulin could suppress Sepp1 expression in the liver under normal insulin action.
One of the mechanisms is through attenuating the action of peroxisomal proliferator-activated receptor-? coactivator-1? (PGC-1?) [43], which is the key regulator of hepatic Sepp1 [44]. However, in three mouse diabetes models of insulin action deficiency, including streptozotocin-induced diabetes and liver insulin-receptor knockout, the expression of PGC-1? was strongly induced [45], which could lead to increased Sepp1 expression. Hence, Sepp1 may be overexpressed under diabetic conditions, whether in an insulin deficiency or insulin resistance. Associations of selenium status with cardiometabolic risk factors: An 8-year follow-up analysis of the olivetti heart study. Plasma selenium and risk of dysglycemia in an elderly french population: Results from the prospective epidemiology of vascular ageing study. A randomized trial of selenium supplementation and risk of type-2 diabetes, as assessed by plasma adiponectin. Regulation of Hepatic Sepp1 Expression by Factors Related to Glucose MetabolismSteinbrenner et al. Effect of selenium and vitamin E on risk of prostate cancer and other cancers: The selenium and vitamin e cancer prevention trial (select). The interaction between forkhead box protein class O1a (FoxO1a) and PGC-1? is of crucial importance for transcriptional regulation of the above two enzymes [43,45]; they also stimulate Sepp1 expression in liver [44]. A binding site for the FoxO1a transcription factor located in Sepp1 promoter has been identified; it is in close proximity to a binding site for hepatocyte nuclear factor 4? (HNF-4?) [44,45,53]. Vitamin E and the risk of prostate cancer: The selenium and vitamin e cancer prevention trial (select). High-level transcription of the Sepp1 gene in liver is ensured by the combined action of FoxO1a and HNF-4? with the coactivator (PGC)-1?.
The evidence suggests that Sepp1 should be negatively regulated by insulin in the liver in the situation of normal insulin sensitivity. Effects of long-term selenium supplementation on the incidence of type 2 diabetes: A randomized trial.
We hypothesize that there could be a feedback regulation between hepatic Sepp1 and pancreatic insulin: in the normal organism, circulating high-glucose concentration stimulates the expression of insulin in the pancreas and Sepp1 in the liver.
The increasing Sepp1 is transported into the pancreas and may collaterally enhance insulin production, as glucose tolerance tests revealed that blood insulin levels were significantly elevated at 0 min in SEPP1-injected mice in the study of Misu and colleagues [42].
Then sufficient insulin may feedback to inhibit hepatic Sepp1 expression as if it was a gluconeogenic enzyme, to maintain glucose homeostasis (Figure 1). However, if insulin resistance is present, normal insulin signaling would be impaired in hepatocytes leading to failure to suppress Sepp1 expression as well as that of gluconeogenic enzymes. Eventually, Sepp1 and gluconeogenic enzymes will be over-produced and secreted, further increasing the blood glucose level. Hence, we think that the increase in circulating Sepp1 could be the result rather than the cause of abnormal glucose metabolism. Serum selenoprotein P levels in patients with type 2 diabetes and prediabetes: Implications for insulin resistance, inflammation, and atherosclerosis. Inverse correlation between serum levels of selenoprotein P and adiponectin in patients with type 2 diabetes.



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