scholarly journals Involvement of communication system between brain and peripheral tissues on the development of post-ischemic glucose intolerance induced by cerebral neuronal damage

2016 ◽  
Vol 148 (1) ◽  
pp. 34-38
Author(s):  
Shinichi Harada ◽  
Shogo Tokuyama
Keyword(s):  
Glucose Intolerance ◽  
Communication System ◽  
Neuronal Damage ◽  
Peripheral Tissues

RETRACTED ARTICLE: Honokiol suppresses the development of post-ischemic glucose intolerance and neuronal damage in mice

2012 ◽  
Vol 66 (4) ◽  
pp. 591-599 ◽  
Author(s):  
Shinichi Harada ◽  
Maya Kishimoto ◽  
Mana Kobayashi ◽  
Kazuo Nakamoto ◽  
Wakako Fujita-Hamabe ◽  
...  
Keyword(s):  
Glucose Intolerance ◽  
Neuronal Damage ◽  
Retracted Article

The development of glucose intolerance after focal cerebral ischemia participates in subsequent neuronal damage

2009 ◽  
Vol 1279 ◽  
pp. 174-181 ◽  
Author(s):  
Shinichi Harada ◽  
Wakako Fujita (Hamabe) ◽  
Kanako Shichi ◽  
Shogo Tokuyama
Keyword(s):  
Cerebral Ischemia ◽  
Glucose Intolerance ◽  
Neuronal Damage ◽  
Focal Cerebral Ischemia

scholarly journals Mechanism of glucose intolerance in mice with dominant negative mutation of CEACAM1

2006 ◽  
Vol 291 (3) ◽  
pp. E517-E524 ◽  
Author(s):  
So-Young Park ◽  
You-Ree Cho ◽  
Hyo-Jeong Kim ◽  
Eun-Gyoung Hong ◽  
Takamasa Higashimori ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Lipid Metabolism ◽  
Glucose Intolerance ◽  
Fatty Acid Synthase ◽  
Visceral Obesity ◽  
Dominant Negative ◽  
Whole Body ◽  
Peripheral Tissues ◽  
Dominant Negative Mutation ◽  
Altered Glucose

Mice with liver-specific overexpression of dominant negative phosphorylation-defective S503A-CEACAM1 mutant (L-SACC1) developed chronic hyperinsulinemia resulting from blunted hepatic clearance of insulin, visceral obesity, and glucose intolerance. To determine the underlying mechanism of altered glucose homeostasis, a 2-h hyperinsulinemic euglycemic clamp was performed, and tissue-specific glucose and lipid metabolism was assessed in awake L-SACC1 and wild-type mice. Inactivation of carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) caused insulin resistance in liver that was mostly due to increased expression of fatty acid synthase and lipid metabolism, resulting in elevated intrahepatic levels of triglyceride and long-chain acyl-CoAs. Whole body insulin resistance in the L-SACC1 mice was further attributed to defects in insulin-stimulated glucose uptake in skeletal muscle and adipose tissue. Insulin resistance in peripheral tissues was associated with significantly elevated intramuscular fat contents that may be secondary to increased whole body adiposity (assessed by 1H-MRS) in the L-SACC1 mice. Overall, these results demonstrate that L-SACC1 is a mouse model in which chronic hyperinsulinemia acts as a cause, and not a consequence, of insulin resistance. Our findings further indicate the important role of CEACAM1 and hepatic insulin clearance in the pathogenesis of obesity and insulin resistance.

Morinda citrifolia fruit juice prevents ischemic neuronal damage through suppression of the development of post-ischemic glucose intolerance

2010 ◽  
Vol 64 (4) ◽  
pp. 468-473 ◽  
Author(s):  
Shinichi Harada ◽  
Wakako Fujita-Hamabe ◽  
Kohei Kamiya ◽  
Yoshiyuki Mizushina ◽  
Toshiko Satake ◽  
...  
Keyword(s):  
Glucose Intolerance ◽  
Fruit Juice ◽  
Neuronal Damage ◽  
Morinda Citrifolia

Do calcium and magnesium deficiencies in reproducing ewes contribute to high lamb mortality?

2020 ◽  
Vol 60 (6) ◽  
pp. 733 ◽  
Author(s):  
Michael A. Friend ◽  
Marie S. Bhanugopan ◽  
Shawn R. McGrath ◽  
Janelle Hocking Edwards ◽  
Serina Hancock ◽  
...  
Keyword(s):  
Neuronal Damage ◽  
Direct Role ◽  
Peripheral Tissues ◽  
Poor Glycaemic Control ◽  
Smooth Muscle Function ◽  
Welfare Problem ◽  
Australian Sheep ◽  
Temperate Pastures ◽  
Lamb Survival ◽  
High Concentrations

High lamb mortality continues to be a significant economic and welfare problem within the Australian sheep industry, with 20–30% of lambs born in commercial flocks dying mostly within 3 days of birth. Clinical hypocalcaemia and hypomagnesaemia cause ewe mortality, and, subsequently, either fetal or lamb death, but it is not known whether subclinical deficiencies of calcium (Ca) and magnesium (Mg) compromise lamb survival. This review considers the potential mechanisms through which Ca and Mg deficiencies may influence lamb survival, and factors influencing the risk of deficiency. Pastures grazed by lambing ewes may be marginal in calcium (Ca; <4 g/kg DM) and magnesium (Mg; <0.9 g/kg DM) but also have a high dietary cation–anion difference (>12 meq/100 g DM) and high concentrations of potassium (K; >30 g/kg DM) and nitrogen. In young cereal crops, sodium concentrations are also often low (<0.9 g/kg DM). This combination of minerals and other nutrients creates an imbalance in supply and increases susceptibility to acute Ca (hypocalcaemia) and Mg (hypomagnesaemia) deficiency. Calcium is required for smooth muscle function and has a direct role in uterine contraction, so may influence the duration of parturition. Low Ca and Mg intake both influence insulin release and sensitivity, low Mg results in poor glycaemic control and insulin resistance by impairing both insulin secretion and its action on peripheral tissues, also potentially altering the duration of parturition as well as risk of metabolic disease. Magnesium is also a neuroprotectant that slows the neuronal damage during hypoxia and has been linked with thermogenesis in offspring and increased immunoglobulins in colostrum. These functions indicate potential importance in improving the ease of parturition and improved ability of the newborn lamb to thermoregulate and survive after birth. Subclinical Ca and Mg deficiencies commonly occur in 20% of lambing ewes grazing temperate pastures, so further studies are warranted to investigate whether correction of these deficiencies can improve lamb survival.

scholarly journals Retraction Note to: Honokiol suppresses the development of post-ischemic glucose intolerance and neuronal damage in mice

2020 ◽  
Vol 74 (3) ◽  
pp. 618-618
Author(s):  
Shinichi Harada ◽  
Maya Kishimoto ◽  
Mana Kobayashi ◽  
Kazuo Nakamoto ◽  
Wakako Fujita-Hamabe ◽  
...  
Keyword(s):  
Glucose Intolerance ◽  
Neuronal Damage
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