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Mass+Spectrometry
Numéro de catalogue:
(BOSSBS-0038R-A488)
Fournisseur:
Bioss
Description:
Glucagon plays a key role in glucose metabolism and homeostasis. Regulates blood glucose by increasing gluconeogenesis and decreasing glycolysis. A counterregulatory hormone of insulin, raises plasma glucose levels in response to insulin-induced hypoglycemia. Plays an important role in initiating and maintaining hyperglycemic conditions in diabetes. GLP-1 is a potent stimulator of glucose-dependent insulin release. Play important roles on gastric motility and the suppression of plasma glucagon levels. May be involved in the suppression of satiety and stimulation of glucose disposal in peripheral tissues, independent of the actions of insulin. Have growth-promoting activities on intestinal epithelium. May also regulate the hypothalamic pituitary axis (HPA) via effects on LH, TSH, CRH, oxytocin, and vasopressin secretion. Increases islet mass through stimulation of islet neogenesis and pancreatic beta cell proliferation. Inhibits beta cell apoptosis. GLP-2 stimulates intestinal growth and up-regulates villus height in the small intestine, concomitant with increased crypt cell proliferation and decreased enterocyte apoptosis. The gastrointestinal tract, from the stomach to the colon is the principal target for GLP-2 action. Plays a key role in nutrient homeostasis, enhancing nutrient assimilation through enhanced gastrointestinal function, as well as increasing nutrient disposal. Stimulates intestinal glucose transport and decreases mucosal permeability. Oxyntomodulin significantly reduces food intake. Inhibits gastric emptying in humans. Suppression of gastric emptying may lead to increased gastric distension, which may contribute to satiety by causing a sensation of fullness. Glicentin may modulate gastric acid secretion and the gastro-pyloro-duodenal activity. May play an important role in intestinal mucosal growth in the early period of life.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-1302R-CY5)
Fournisseur:
Bioss
Description:
Glutamic Acid Decarboxylase (GAD) catalyzes the conversion of L glutamate to g-aminobutyric acid (GABA), the principal inhibitory neurotransmitter in the brain, and a putative paracrine signal molecule in pancreatic islets. GAD has a restricted tissue distribution. It is highly expressed in the cytoplasm of GABAergic neurons in the central nervous system (CNS) and pancreatic beta cells. It is also present in other non-neuronal tissues such as testis, oviduct and ovary. GAD is also transiently expressed in non-GABAergic cells of the embryonic and adult nervous system, suggesting its involvement in development and plasticity. GAD exists as two isoforms, GAD65 and GAD67 (molecular masses of 65 and 67 kD, respectively) that are encoded by two different genes. GAD65 is an ampiphilic, membraneanchored protein, (585 amino acid residues) and is encoded on human chromosome 10. GAD67 is a cytoplasmic protein (594 amino acid residues) and is encoded on chromosome 2. There is 64% amino acid identity between the two isoforms, with the highest diversity located at the N terminus, which in GAD65 is required for targeting the enzyme to GABA-containing secretory vesicles. The two isoforms appear to have distinct intraneuronal distribution in the brain. GAD65 has been identified as an autoantigen in insulindependent diabetes mellitus (IDDM) and stiff-man syndrome (SMS), IDDM is an autoimmune disease that results from T cell mediated destruction of pancreatic insulin-secreting beta cells. Islet-reactive T cells and primarily to GAD65 (also named beta cell autoantigen) can be detected in peripheral blood of 80% of recent-onset IDD patients and in pre-diabetic high-risk subjects before onset of clinical symptoms. This suggests that GAD may be an important marker in the early stages of the disease.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-1302R-CY7)
Fournisseur:
Bioss
Description:
Glutamic Acid Decarboxylase (GAD) catalyzes the conversion of L glutamate to g-aminobutyric acid (GABA), the principal inhibitory neurotransmitter in the brain, and a putative paracrine signal molecule in pancreatic islets. GAD has a restricted tissue distribution. It is highly expressed in the cytoplasm of GABAergic neurons in the central nervous system (CNS) and pancreatic beta cells. It is also present in other non-neuronal tissues such as testis, oviduct and ovary. GAD is also transiently expressed in non-GABAergic cells of the embryonic and adult nervous system, suggesting its involvement in development and plasticity. GAD exists as two isoforms, GAD65 and GAD67 (molecular masses of 65 and 67 kD, respectively) that are encoded by two different genes. GAD65 is an ampiphilic, membraneanchored protein, (585 amino acid residues) and is encoded on human chromosome 10. GAD67 is a cytoplasmic protein (594 amino acid residues) and is encoded on chromosome 2. There is 64% amino acid identity between the two isoforms, with the highest diversity located at the N terminus, which in GAD65 is required for targeting the enzyme to GABA-containing secretory vesicles. The two isoforms appear to have distinct intraneuronal distribution in the brain. GAD65 has been identified as an autoantigen in insulindependent diabetes mellitus (IDDM) and stiff-man syndrome (SMS), IDDM is an autoimmune disease that results from T cell mediated destruction of pancreatic insulin-secreting beta cells. Islet-reactive T cells and primarily to GAD65 (also named beta cell autoantigen) can be detected in peripheral blood of 80% of recent-onset IDD patients and in pre-diabetic high-risk subjects before onset of clinical symptoms. This suggests that GAD may be an important marker in the early stages of the disease.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-5855R-A350)
Fournisseur:
Bioss
Description:
ADAM32 was first discovered in a search for testis-specific proteinases. ADAM32 was identified in human, rat, mouse, macaque and chimp, and thus far has been found only in testis. In mice, ADAM32 is found on the sperm surface, where it may play a role in fertilization. ADAM32 is a member of the ADAMs family (A Disintegrin And Metalloproteinase), but does not contain the canonical HExxHxxxxH zinc-binding metalloproteinase catalytic site. The domain structure of the full length ADAM32 includes a signal sequence, propeptide domain, metalloproteinase-like domain, disintegrin-like domain, cys-rich domain, EGF-like domain, a short spacer region, then the transmembrane domain and a cytoplasmic domain. Like many of the reproductive-specific ADAMS, ADAM32 plays a non-enzymatic role, or (as is the case for ADAMs 1 & 2 (fertilin alpha and beta)), the protein acts in concert with a proteolytically active ADAM to process proteins. Little is known about interactions between ADAM32 and other ADAMs. Several different sequences for human ADAM32 are published; 787, 688, 649, 629, and 279 amino acids in length. The 688 amino acid form is identical to the 787 AA form until the EGF-like domain, and lacks the TM and cytoplasmic domains. The 649 AA form is likewise identical to the longer form, just to the start of the TM domain, and also lacks the TM and cytoplasmic domains. The 629 AA form has a deletion of 107 residues midway into the MP-like domain, and lacks the amino end of the disintegrin domain, but contains the rest of the domains found in the full-length ADAM32. The predicted masses for the different versions are 87.8, 76.9, 72.9, 70.9 and 32.1, respectively, for the 786, 688, 649, 629 and 279 AA forms.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-3796R-CY5.5)
Fournisseur:
Bioss
Description:
Glucagon plays a key role in glucose metabolism and homeostasis. Regulates blood glucose by increasing gluconeogenesis and decreasing glycolysis. A counterregulatory hormone of insulin, raises plasma glucose levels in response to insulin-induced hypoglycemia. Plays an important role in initiating and maintaining hyperglycemic conditions in diabetes. GLP-1 is a potent stimulator of glucose-dependent insulin release. Play important roles on gastric motility and the suppression of plasma glucagon levels. May be involved in the suppression of satiety and stimulation of glucose disposal in peripheral tissues, independent of the actions of insulin. Have growth-promoting activities on intestinal epithelium. May also regulate the hypothalamic pituitary axis (HPA) via effects on LH, TSH, CRH, oxytocin, and vasopressin secretion. Increases islet mass through stimulation of islet neogenesis and pancreatic beta cell proliferation. Inhibits beta cell apoptosis. GLP-2 stimulates intestinal growth and up-regulates villus height in the small intestine, concomitant with increased crypt cell proliferation and decreased enterocyte apoptosis. The gastrointestinal tract, from the stomach to the colon is the principal target for GLP-2 action. Plays a key role in nutrient homeostasis, enhancing nutrient assimilation through enhanced gastrointestinal function, as well as increasing nutrient disposal. Stimulates intestinal glucose transport and decreases mucosal permeability. Oxyntomodulin significantly reduces food intake. Inhibits gastric emptying in humans. Suppression of gastric emptying may lead to increased gastric distension, which may contribute to satiety by causing a sensation of fullness. Glicentin may modulate gastric acid secretion and the gastro-pyloro-duodenal activity. May play an important role in intestinal mucosal growth in the early period of life.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-0038R-CY7)
Fournisseur:
Bioss
Description:
Glucagon plays a key role in glucose metabolism and homeostasis. Regulates blood glucose by increasing gluconeogenesis and decreasing glycolysis. A counterregulatory hormone of insulin, raises plasma glucose levels in response to insulin-induced hypoglycemia. Plays an important role in initiating and maintaining hyperglycemic conditions in diabetes. GLP-1 is a potent stimulator of glucose-dependent insulin release. Play important roles on gastric motility and the suppression of plasma glucagon levels. May be involved in the suppression of satiety and stimulation of glucose disposal in peripheral tissues, independent of the actions of insulin. Have growth-promoting activities on intestinal epithelium. May also regulate the hypothalamic pituitary axis (HPA) via effects on LH, TSH, CRH, oxytocin, and vasopressin secretion. Increases islet mass through stimulation of islet neogenesis and pancreatic beta cell proliferation. Inhibits beta cell apoptosis. GLP-2 stimulates intestinal growth and up-regulates villus height in the small intestine, concomitant with increased crypt cell proliferation and decreased enterocyte apoptosis. The gastrointestinal tract, from the stomach to the colon is the principal target for GLP-2 action. Plays a key role in nutrient homeostasis, enhancing nutrient assimilation through enhanced gastrointestinal function, as well as increasing nutrient disposal. Stimulates intestinal glucose transport and decreases mucosal permeability. Oxyntomodulin significantly reduces food intake. Inhibits gastric emptying in humans. Suppression of gastric emptying may lead to increased gastric distension, which may contribute to satiety by causing a sensation of fullness. Glicentin may modulate gastric acid secretion and the gastro-pyloro-duodenal activity. May play an important role in intestinal mucosal growth in the early period of life.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-13736R-CY5)
Fournisseur:
Bioss
Description:
ADAM13 was first described as a protein expressed in somatic mesoderm and neural crest cells, in developing Xenopus embryos. ADAM13 was also found in liver, heart, and intestines from adult Xenopus. ADAM13 may regulate cellular signaling via Src and Src tyrosine kinase. ADAM13 may also act as a cell attachment molecule, by binding integrins through the cysteine rich domain amoung many other roles. A member of the metalloproteinase family containing disintegrin like domains (ADAMs) the functions of ADAM13 are still poorly understood. ADAM13 contains the canonical HExxHxxxxxH zinc metalloproteinase motif, as well as disintegrin, cysteine rich, EFG like, transmembrane and Cytoplasmic domains. ADAM13 has been shown to be proteolytically active, cleaving fibronectin after binding it to the EGF like domain. ADAM13 is also shed from cells in culture, cleaved aminoterminal from the transmembrane domain, and is released into the culture media. Shed ADAM13 is a 52 kD protein, and can form complexes with a2 macroglobulin, suggesting it is a competent protease. Xenopus ADAM13 has greatest homology with human ADAM 33 (51% identical), and is 46% identical with human or mouse ADAM12 or ADAM19. It is still unclear if any of these ADAMs are species orthologs of Xenopus ADAM13, but there are significant differences between the related sequences, suggesting that ADAM13 may be a unique protein. The full length Xenopus ADAM13 sequence codes for a 914 amino acid protein. Predicted mass is 99.749 kD, but glycosylation and cyteine rich regions give Xenopus ADAM13 an apparent MW of 120 kD unprocessed, and 97 kD processed forms, on reduced SDS PAGE gels. ADAM13 contains a putative furin cleavage site, suggesting that a prohormone convertase cleaves the propeptide domain away from the catalytic domain
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-13736R-HRP)
Fournisseur:
Bioss
Description:
ADAM13 was first described as a protein expressed in somatic mesoderm and neural crest cells, in developing Xenopus embryos. ADAM13 was also found in liver, heart, and intestines from adult Xenopus. ADAM13 may regulate cellular signaling via Src and Src tyrosine kinase. ADAM13 may also act as a cell attachment molecule, by binding integrins through the cysteine rich domain amoung many other roles. A member of the metalloproteinase family containing disintegrin like domains (ADAMs) the functions of ADAM13 are still poorly understood. ADAM13 contains the canonical HExxHxxxxxH zinc metalloproteinase motif, as well as disintegrin, cysteine rich, EFG like, transmembrane and Cytoplasmic domains. ADAM13 has been shown to be proteolytically active, cleaving fibronectin after binding it to the EGF like domain. ADAM13 is also shed from cells in culture, cleaved aminoterminal from the transmembrane domain, and is released into the culture media. Shed ADAM13 is a 52 kD protein, and can form complexes with a2 macroglobulin, suggesting it is a competent protease. Xenopus ADAM13 has greatest homology with human ADAM 33 (51% identical), and is 46% identical with human or mouse ADAM12 or ADAM19. It is still unclear if any of these ADAMs are species orthologs of Xenopus ADAM13, but there are significant differences between the related sequences, suggesting that ADAM13 may be a unique protein. The full length Xenopus ADAM13 sequence codes for a 914 amino acid protein. Predicted mass is 99.749 kD, but glycosylation and cyteine rich regions give Xenopus ADAM13 an apparent MW of 120 kD unprocessed, and 97 kD processed forms, on reduced SDS PAGE gels. ADAM13 contains a putative furin cleavage site, suggesting that a prohormone convertase cleaves the propeptide domain away from the catalytic domain
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-0933R-CY5)
Fournisseur:
Bioss
Description:
Glucagon plays a key role in glucose metabolism and homeostasis. Regulates blood glucose by increasing gluconeogenesis and decreasing glycolysis. A counterregulatory hormone of insulin, raises plasma glucose levels in response to insulin-induced hypoglycemia. Plays an important role in initiating and maintaining hyperglycemic conditions in diabetes. GLP-1 is a potent stimulator of glucose-dependent insulin release. Play important roles on gastric motility and the suppression of plasma glucagon levels. May be involved in the suppression of satiety and stimulation of glucose disposal in peripheral tissues, independent of the actions of insulin. Have growth-promoting activities on intestinal epithelium. May also regulate the hypothalamic pituitary axis (HPA) via effects on LH, TSH, CRH, oxytocin, and vasopressin secretion. Increases islet mass through stimulation of islet neogenesis and pancreatic beta cell proliferation. Inhibits beta cell apoptosis. GLP-2 stimulates intestinal growth and up-regulates villus height in the small intestine, concomitant with increased crypt cell proliferation and decreased enterocyte apoptosis. The gastrointestinal tract, from the stomach to the colon is the principal target for GLP-2 action. Plays a key role in nutrient homeostasis, enhancing nutrient assimilation through enhanced gastrointestinal function, as well as increasing nutrient disposal. Stimulates intestinal glucose transport and decreases mucosal permeability. Oxyntomodulin significantly reduces food intake. Inhibits gastric emptying in humans. Suppression of gastric emptying may lead to increased gastric distension, which may contribute to satiety by causing a sensation of fullness. Glicentin may modulate gastric acid secretion and the gastro-pyloro-duodenal activity. May play an important role in intestinal mucosal growth in the early period of life.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-2766R-A750)
Fournisseur:
Bioss
Description:
FOXO1 is a transcription factor that is the main target of insulin signaling and regulates metabolic homeostasis in response to oxidative stress. Binds to the insulin response element (IRE) with consensus sequence 5'-TT[G/A]TTTTG-3' and the related Daf-16 family binding element (DBE) with consensus sequence 5'-TT[G/A]TTTAC-3'. Activity suppressed by insulin. Main regulator of redox balance and osteoblast numbers and controls bone mass. Orchestrates the endocrine function of the skeleton in regulating glucose metabolism. Acts synergistically with ATF4 to suppress osteocalcin/BGLAP activity, increasing glucose levels and triggering glucose intolerance and insulin insensitivity. Also suppresses the transcriptional activity of RUNX2, an upstream activator of osteocalcin/BGLAP. In hepatocytes, promotes gluconeogenesis by acting together with PPARGC1A and CEBPA to activate the expression of genes such as IGFBP1, G6PC and PCK1. Important regulator of cell death acting downstream of CDK1, PKB/AKT1 and STK4/MST1. Promotes neural cell death. Mediates insulin action on adipose tissue. Regulates the expression of adipogenic genes such as PPARG during preadipocyte differentiation and, adipocyte size and adipose tissue-specific gene expression in response to excessive calorie intake. Regulates the transcriptional activity of GADD45A and repair of nitric oxide-damaged DNA in beta-cells. Required for the autophagic cell death induction in response to starvation or oxidative stress in a transcription-independent manner.
FOXO4 is a forkhead transcription factor involved in the regulation of the insulin signaling pathway. It binds to insulin-response elements (IREs) and can activate transcription of IGFBP1. FOXO4 down-regulates expression of HIF1A and suppresses hypoxia-induced transcriptional activation of HIF1A-modulated genes. It is also involved in negative regulation of the cell cycle.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-1302R-A488)
Fournisseur:
Bioss
Description:
Glutamic Acid Decarboxylase (GAD) catalyzes the conversion of L glutamate to g-aminobutyric acid (GABA), the principal inhibitory neurotransmitter in the brain, and a putative paracrine signal molecule in pancreatic islets. GAD has a restricted tissue distribution. It is highly expressed in the cytoplasm of GABAergic neurons in the central nervous system (CNS) and pancreatic beta cells. It is also present in other non-neuronal tissues such as testis, oviduct and ovary. GAD is also transiently expressed in non-GABAergic cells of the embryonic and adult nervous system, suggesting its involvement in development and plasticity. GAD exists as two isoforms, GAD65 and GAD67 (molecular masses of 65 and 67 kD, respectively) that are encoded by two different genes. GAD65 is an ampiphilic, membraneanchored protein, (585 amino acid residues) and is encoded on human chromosome 10. GAD67 is a cytoplasmic protein (594 amino acid residues) and is encoded on chromosome 2. There is 64% amino acid identity between the two isoforms, with the highest diversity located at the N terminus, which in GAD65 is required for targeting the enzyme to GABA-containing secretory vesicles. The two isoforms appear to have distinct intraneuronal distribution in the brain. GAD65 has been identified as an autoantigen in insulindependent diabetes mellitus (IDDM) and stiff-man syndrome (SMS), IDDM is an autoimmune disease that results from T cell mediated destruction of pancreatic insulin-secreting beta cells. Islet-reactive T cells and primarily to GAD65 (also named beta cell autoantigen) can be detected in peripheral blood of 80% of recent-onset IDD patients and in pre-diabetic high-risk subjects before onset of clinical symptoms. This suggests that GAD may be an important marker in the early stages of the disease.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-5855R-A555)
Fournisseur:
Bioss
Description:
ADAM32 was first discovered in a search for testis-specific proteinases. ADAM32 was identified in human, rat, mouse, macaque and chimp, and thus far has been found only in testis. In mice, ADAM32 is found on the sperm surface, where it may play a role in fertilization. ADAM32 is a member of the ADAMs family (A Disintegrin And Metalloproteinase), but does not contain the canonical HExxHxxxxH zinc-binding metalloproteinase catalytic site. The domain structure of the full length ADAM32 includes a signal sequence, propeptide domain, metalloproteinase-like domain, disintegrin-like domain, cys-rich domain, EGF-like domain, a short spacer region, then the transmembrane domain and a cytoplasmic domain. Like many of the reproductive-specific ADAMS, ADAM32 plays a non-enzymatic role, or (as is the case for ADAMs 1 & 2 (fertilin alpha and beta)), the protein acts in concert with a proteolytically active ADAM to process proteins. Little is known about interactions between ADAM32 and other ADAMs. Several different sequences for human ADAM32 are published; 787, 688, 649, 629, and 279 amino acids in length. The 688 amino acid form is identical to the 787 AA form until the EGF-like domain, and lacks the TM and cytoplasmic domains. The 649 AA form is likewise identical to the longer form, just to the start of the TM domain, and also lacks the TM and cytoplasmic domains. The 629 AA form has a deletion of 107 residues midway into the MP-like domain, and lacks the amino end of the disintegrin domain, but contains the rest of the domains found in the full-length ADAM32. The predicted masses for the different versions are 87.8, 76.9, 72.9, 70.9 and 32.1, respectively, for the 786, 688, 649, 629 and 279 AA forms.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-0933R-CY3)
Fournisseur:
Bioss
Description:
Glucagon plays a key role in glucose metabolism and homeostasis. Regulates blood glucose by increasing gluconeogenesis and decreasing glycolysis. A counterregulatory hormone of insulin, raises plasma glucose levels in response to insulin-induced hypoglycemia. Plays an important role in initiating and maintaining hyperglycemic conditions in diabetes. GLP-1 is a potent stimulator of glucose-dependent insulin release. Play important roles on gastric motility and the suppression of plasma glucagon levels. May be involved in the suppression of satiety and stimulation of glucose disposal in peripheral tissues, independent of the actions of insulin. Have growth-promoting activities on intestinal epithelium. May also regulate the hypothalamic pituitary axis (HPA) via effects on LH, TSH, CRH, oxytocin, and vasopressin secretion. Increases islet mass through stimulation of islet neogenesis and pancreatic beta cell proliferation. Inhibits beta cell apoptosis. GLP-2 stimulates intestinal growth and up-regulates villus height in the small intestine, concomitant with increased crypt cell proliferation and decreased enterocyte apoptosis. The gastrointestinal tract, from the stomach to the colon is the principal target for GLP-2 action. Plays a key role in nutrient homeostasis, enhancing nutrient assimilation through enhanced gastrointestinal function, as well as increasing nutrient disposal. Stimulates intestinal glucose transport and decreases mucosal permeability. Oxyntomodulin significantly reduces food intake. Inhibits gastric emptying in humans. Suppression of gastric emptying may lead to increased gastric distension, which may contribute to satiety by causing a sensation of fullness. Glicentin may modulate gastric acid secretion and the gastro-pyloro-duodenal activity. May play an important role in intestinal mucosal growth in the early period of life.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-0933R-A350)
Fournisseur:
Bioss
Description:
Glucagon plays a key role in glucose metabolism and homeostasis. Regulates blood glucose by increasing gluconeogenesis and decreasing glycolysis. A counterregulatory hormone of insulin, raises plasma glucose levels in response to insulin-induced hypoglycemia. Plays an important role in initiating and maintaining hyperglycemic conditions in diabetes. GLP-1 is a potent stimulator of glucose-dependent insulin release. Play important roles on gastric motility and the suppression of plasma glucagon levels. May be involved in the suppression of satiety and stimulation of glucose disposal in peripheral tissues, independent of the actions of insulin. Have growth-promoting activities on intestinal epithelium. May also regulate the hypothalamic pituitary axis (HPA) via effects on LH, TSH, CRH, oxytocin, and vasopressin secretion. Increases islet mass through stimulation of islet neogenesis and pancreatic beta cell proliferation. Inhibits beta cell apoptosis. GLP-2 stimulates intestinal growth and up-regulates villus height in the small intestine, concomitant with increased crypt cell proliferation and decreased enterocyte apoptosis. The gastrointestinal tract, from the stomach to the colon is the principal target for GLP-2 action. Plays a key role in nutrient homeostasis, enhancing nutrient assimilation through enhanced gastrointestinal function, as well as increasing nutrient disposal. Stimulates intestinal glucose transport and decreases mucosal permeability. Oxyntomodulin significantly reduces food intake. Inhibits gastric emptying in humans. Suppression of gastric emptying may lead to increased gastric distension, which may contribute to satiety by causing a sensation of fullness. Glicentin may modulate gastric acid secretion and the gastro-pyloro-duodenal activity. May play an important role in intestinal mucosal growth in the early period of life.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-0208R-A680)
Fournisseur:
Bioss
Description:
Glucagon plays a key role in glucose metabolism and homeostasis. Regulates blood glucose by increasing gluconeogenesis and decreasing glycolysis. A counterregulatory hormone of insulin, raises plasma glucose levels in response to insulin-induced hypoglycemia. Plays an important role in initiating and maintaining hyperglycemic conditions in diabetes. GLP-1 is a potent stimulator of glucose-dependent insulin release. Play important roles on gastric motility and the suppression of plasma glucagon levels. May be involved in the suppression of satiety and stimulation of glucose disposal in peripheral tissues, independent of the actions of insulin. Have growth-promoting activities on intestinal epithelium. May also regulate the hypothalamic pituitary axis (HPA) via effects on LH, TSH, CRH, oxytocin, and vasopressin secretion. Increases islet mass through stimulation of islet neogenesis and pancreatic beta cell proliferation. Inhibits beta cell apoptosis. GLP-2 stimulates intestinal growth and up-regulates villus height in the small intestine, concomitant with increased crypt cell proliferation and decreased enterocyte apoptosis. The gastrointestinal tract, from the stomach to the colon is the principal target for GLP-2 action. Plays a key role in nutrient homeostasis, enhancing nutrient assimilation through enhanced gastrointestinal function, as well as increasing nutrient disposal. Stimulates intestinal glucose transport and decreases mucosal permeability. Oxyntomodulin significantly reduces food intake. Inhibits gastric emptying in humans. Suppression of gastric emptying may lead to increased gastric distension, which may contribute to satiety by causing a sensation of fullness. Glicentin may modulate gastric acid secretion and the gastro-pyloro-duodenal activity. May play an important role in intestinal mucosal growth in the early period of life.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-0208R-FITC)
Fournisseur:
Bioss
Description:
Glucagon plays a key role in glucose metabolism and homeostasis. Regulates blood glucose by increasing gluconeogenesis and decreasing glycolysis. A counterregulatory hormone of insulin, raises plasma glucose levels in response to insulin-induced hypoglycemia. Plays an important role in initiating and maintaining hyperglycemic conditions in diabetes. GLP-1 is a potent stimulator of glucose-dependent insulin release. Play important roles on gastric motility and the suppression of plasma glucagon levels. May be involved in the suppression of satiety and stimulation of glucose disposal in peripheral tissues, independent of the actions of insulin. Have growth-promoting activities on intestinal epithelium. May also regulate the hypothalamic pituitary axis (HPA) via effects on LH, TSH, CRH, oxytocin, and vasopressin secretion. Increases islet mass through stimulation of islet neogenesis and pancreatic beta cell proliferation. Inhibits beta cell apoptosis. GLP-2 stimulates intestinal growth and up-regulates villus height in the small intestine, concomitant with increased crypt cell proliferation and decreased enterocyte apoptosis. The gastrointestinal tract, from the stomach to the colon is the principal target for GLP-2 action. Plays a key role in nutrient homeostasis, enhancing nutrient assimilation through enhanced gastrointestinal function, as well as increasing nutrient disposal. Stimulates intestinal glucose transport and decreases mucosal permeability. Oxyntomodulin significantly reduces food intake. Inhibits gastric emptying in humans. Suppression of gastric emptying may lead to increased gastric distension, which may contribute to satiety by causing a sensation of fullness. Glicentin may modulate gastric acid secretion and the gastro-pyloro-duodenal activity. May play an important role in intestinal mucosal growth in the early period of life.
UOM:
1 * 100 µl
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est toujours affiché et vous avez besoin d'aide, s'il vous plaît appelez-nous au 016 385 011
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