Human Gastric Inhibitory Polypeptide Receptor: Cloning of the Gene (GIPR) and cDNA

Yamada, Yoshio; Hayami, Tadao; Nakamura, Katsuki; Kaisaki, Pamela J.; Someya, Yoshimichi; Wang, Changzheng; Seino, Susumu; Seino, Yutaka

doi:10.1006/geno.1995.9937

Cited by 84 publications

(45 citation statements)

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“…The GIPR deficient model used by Xie et al and Tsukiyama et al possessed a deletion of exons 4 and 5 that encode a portion, but not the totality, of the extracellular domain of the GIPR. Our model of GIPR deficiency consists of a deletion of the first 6 exons, which encode the totality of the extracellular domain and a portion of the first transmembrane helix of the GIPR [35,36]. Although both constructs resulted in non-functional receptors as assessed by cAMP responses, one might argue that the binding affinity of GIP to its receptor might be different between the two constructs and as such the availability of GIP for another splice variant of the receptor might be impaired.…”

Section: Discussionmentioning

confidence: 99%

Glucose-dependent insulinotropic polypeptide receptor deficiency leads to modifications of trabecular bone volume and quality in mice

Gaudin-Audrain¹,

Irwin²,

Mansur³

et al. 2013

Bone

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A role for the gastro-intestinal tract in controlling bone remodeling is suspected since serum levels of bone remodeling markers are affected rapidly after a meal. Glucose-dependent insulinotropic polypeptide (GIP) represents a suitable candidate in mediating this effect. The aim of the present study was to investigate the effect of total inhibition of GIP signaling on trabecular bone volume, microarchitecture and quality. We used GIP receptor (GIPR) knockout mice and investigated trabecular bone volume and microarchitecture by microCT and histomorphometry. GIPR-deficient animals at 16 weeks of age presented with a significant (20%) increase in trabecular bone mass accompanied by an increase (17%) in trabecular number. In addition, the number of osteoclasts and bone formation rate was significantly reduced and augmented, respectively in these animals when compared with wild-type littermates. These modifications of trabecular bone microarchitecture are linked to a remodeling in the expression pattern of adipokines in the GIPR-deficient mice. On the other hand, despite significant enhancement in bone volume, intrinsic mechanical properties of the bone matrix was reduced as well as the distribution of bone mineral density and the ratio of mature/immature collagen cross-links. Taken together, these results indicate an increase in trabecular bone volume in GIPR KO animals associated with a reduction in bone quality.

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Section: Discussionmentioning

confidence: 99%

Glucose-dependent insulinotropic polypeptide receptor deficiency leads to modifications of trabecular bone volume and quality in mice

Gaudin-Audrain¹,

Irwin²,

Mansur³

et al. 2013

Bone

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“…Receptor cDNAs were subsequently isolated from human (466 amino acid) (Gremlich et al, 1995;Yamada et al, 1995) and hamster (462 amino acids) (Yasuda et al, 1994) cDNA libraries. The human receptor gene, located on chromosomal 19q13.3 (Gremlich et al, 1995), contains 14 exons spanning approximately 14 kb .…”

Section: A Structurementioning

confidence: 99%

International Union of Pharmacology. XXXV. The Glucagon Receptor Family

et al. 2003

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“…However, several studies have failed to detect any mutations in NIDDMpatients, indicating that a primary structural abnormality of amylin or its precursor is not responsible for the formation of the islet amyloid seen in NIDDM patients (91,92). Other candidates are the genes for the receptors for hormones called "grucoincretins" such as GLP-1 (93) and GIP (94), since these hormones have strong potentiating effects on glucose-induced insulin secretion (95) , defects in these receptors at the level ofpancreatic p-cells might lead to impaired glucoseinduced insulin secretion.…”

Section: Insulin Genementioning

confidence: 99%

Recent Progress in the Molecular Genetic Aspects of Non-Insulin-Dependent Diabetes Mellitus.

Seino

1996

Intern. Med.

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SusumuSeinoNon-insulin-dependent diabetes mellitus (NIDDM) is one of the most commonmetabolic and endocrine disorders in developed countries. NIDDMis a multifactorial disorder in which genetic factors play a complex role in its development. Until recently, little has been known of the genetic determinants ofNIDDM.Advances in molecular biological and molecular genetic approaches have now made it possible to begin to identify the diabetes susceptibility genes in NIDDM. This review describes the progress of recent research in the molecular genetic aspects of NIDDM. (Internal Medicine 35: 347-355, 1996)

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Human Gastric Inhibitory Polypeptide Receptor: Cloning of the Gene (GIPR) and cDNA

Cited by 84 publications

References 0 publications

Glucose-dependent insulinotropic polypeptide receptor deficiency leads to modifications of trabecular bone volume and quality in mice

Glucose-dependent insulinotropic polypeptide receptor deficiency leads to modifications of trabecular bone volume and quality in mice

International Union of Pharmacology. XXXV. The Glucagon Receptor Family

Recent Progress in the Molecular Genetic Aspects of Non-Insulin-Dependent Diabetes Mellitus.

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