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1.
Biochem Biophys Res Commun ; 513(4): 974-982, 2019 06 11.
Article in English | MEDLINE | ID: mdl-31003779

ABSTRACT

AIMS/INTRODUCTION: Caloric restriction (CR) promotes longevity and exerts anti-aging effects by increasing Sirtuin production and activation. Gastric inhibitory polypeptide (GIP), a gastrointestinal peptide hormone, exerts various effects on pancreatic ß-cells and extra-pancreatic tissues. GIP promotes glucose-dependent augmentation of insulin secretion and uptake of nutrients into the adipose tissue. MATERIALS AND METHODS: Gipr-/- and Gipr+/+ mice were used for lifespan analysis, behavior experiments and gene expression of adipose tissue and muscles. 3T3-L1 differentiated adipocytes were used for Sirt1 and Nampt expression followed by treatment with GIP and α-lipoic acid. RESULTS: We observed that GIP receptor-knockout (Gipr-/-) mice fed normal diet showed an extended lifespan, increased exploratory and decreased anxiety-based behaviors, which are characteristic behavioral changes under CR. Moreover, Gipr-/- mice showed increased Sirt1 and Nampt expression in the adipose tissue. GIP suppressed α-lipoic acid-induced Sirt1 expression and activity in differentiated adipocytes. CONCLUSIONS: Although maintenance of CR is difficult, food intake and muscle endurance of Gipr-/- mice were similar to those of wild-type mice. Inhibition of GIP signaling may be a novel strategy to extend the lifespan of diabetic patients.


Subject(s)
Caloric Restriction , Gastric Inhibitory Polypeptide/antagonists & inhibitors , Longevity/physiology , Signal Transduction/physiology , 3T3-L1 Cells , Adipocytes/metabolism , Adipose Tissue/metabolism , Animals , Cytokines/metabolism , Mice , Mice, Knockout , Nicotinamide Phosphoribosyltransferase/metabolism , Receptors, Gastrointestinal Hormone/genetics , Sirtuin 1/metabolism
2.
Endocrinology ; 158(7): 2134-2144, 2017 07 01.
Article in English | MEDLINE | ID: mdl-28430907

ABSTRACT

In addition to overeating, starvation also reduces fecundity in mammals. However, little is known about the molecular mechanisms linking food intake to fertility, especially in males. Gastric inhibitory polypeptide (GIP), which is released from intestinal K-cells after meal ingestion, stimulates insulin secretion from pancreatic ß-cells through the action of incretin and has several extrapancreatic effects. Here, we identified GIP receptor (Gipr) expression in mouse spermatids. Microarray analysis revealed that pregnancy-specific glycoprotein 17 (Psg17), a potential CD9-binding partner, was significantly decreased in GIP receptor-knockout (Gipr-/-) testes. Glycosylphosphatidylinositol-anchored PSG17 was expressed on the surface of acrosome-reacted sperm, and Gipr-/- sperm led to a lower fertilization rate in vitro, compared with that of Gipr+/+ sperm, both in the absence and presence of the zona pellucida. Plasma GIP concentrations and Psg17 messenger RNA (mRNA) were immediately increased in the testis after a single meal, whereas ingestion of a chronic high-fat diet markedly decreased Gipr and Psg17 mRNA. These results suggest that reduced GIP signaling, by decreased GIP levels or the downregulation of Gipr, is associated with the reduction of fecundity due to starvation or overeating. Thus, proper regulation of GIP signaling in the testis could be a potential unique therapeutic target for male infertility in obese and diabetic individuals.


Subject(s)
Eating/physiology , Gastric Inhibitory Polypeptide/physiology , Glycoproteins/physiology , Pregnancy Proteins/physiology , Receptors, Gastrointestinal Hormone/physiology , Sperm-Ovum Interactions/genetics , Animals , Female , Fertility/genetics , Gastric Inhibitory Polypeptide/genetics , Glycoproteins/genetics , Intercellular Signaling Peptides and Proteins , Male , Mice , Mice, Inbred C57BL , Mice, Knockout , Microarray Analysis , Pregnancy Proteins/genetics , Receptors, Gastrointestinal Hormone/genetics , Signal Transduction/genetics , Testis/metabolism
3.
Nihon Rinsho ; 70(8): 1445-50, 2012 Aug.
Article in Japanese | MEDLINE | ID: mdl-22894087

ABSTRACT

Diabetes is the chronic progressive disease and blood glucose control mechanism fails for impaired insulin secretion and increased resistance to insulin action in the skeletal muscle and liver. Unfortunately, cure for diabetes cannot be achieved now, however, it may be possible to control blood glucose at the same level compared with non-diabetic individuals by combining treatment methods. Of course, dietary and exercise therapy are important, and oral hypoglycemic agents and insulin will be used appropriately further, to control not only the average of the blood glucose levels for but also the blood glucose change.


Subject(s)
Blood Glucose , Diabetes Mellitus/blood , Diabetes Mellitus/therapy , Hypoglycemic Agents/administration & dosage , Insulin/administration & dosage , Diet, Diabetic , Exercise Therapy , Glycoside Hydrolase Inhibitors , Humans , Hypoglycemic Agents/pharmacology , Incretins/physiology , Insulin/metabolism , Insulin Resistance , Insulin Secretion , Insulin-Secreting Cells/metabolism
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