Effects of Cyclohexanonic Long-Chain Fatty Alcohol, tCFA15 on Amino Acids in Diabetic Rat Brain: A Preliminary Study

Shinbori, Chiko; Shirayama, Yukihiko; Mitani, Hiroaki; Saito, Motoaki; Satoh, Keisuke

doi:10.1007/s11064-008-9611-2

Cited by 4 publications

(4 citation statements)

References 57 publications

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“…We found that cyclohexenonic long-chain fatty alcohol has no effect on serum insulin or glucose levels in streptozotocin-induced diabetic animals, but that it has therapeutic and/or preventive effects on streptozotocin-induced cystopathy, enteropathy, angiopathy, nephropathy, and tracheal dysfunction. Recently, we have also reported that streptozotocin-induced diabetes caused alterations of amino acid components in the central nervous system of rats, and that treatment with cyclohexenonic long-chain fatty alcohol significantly ameliorated these alterations (Shinbori et al, 2008). These reports strongly suggest that cyclohexenonic long-chain fatty alcohol has therapeutic and/or preventive effects on not only peripheral neuropathy but also central neuropathy induced by streptozotocin.…”

Section: Discussionmentioning

confidence: 69%

Characterization of the ileal muscarinic receptor system in 70-week-old type II Goto–Kakizaki diabetic rats; effects of cyclohexenonic long-chain fatty alcohol

Okada¹,

Saito²,

Kinoshita³

et al. 2009

European Journal of Pharmacology

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As gastrointestinal motility disorders are frequently reported in patients with diabetes, we attempted to clarify the effects of cyclohexenonic long-chain fatty alcohol in type 2 Goto-Kakizaki (GK) diabetic enteropathy. At 40 weeks of age male GK rats divided into three groups (treated with 0, 2 or 8 mg/kg of cyclohexenonic long-chain fatty alcohol; started at the age of 40 weeks). Age-matched male Wistar rats were used in this study. At 70 weeks of age the ileal functions were estimated by organ bath studies using 100 mM KCl and carbachol. The expression levels of muscarinic M(2) and M(3) receptor mRNAs in the ileum were investigated by real-time polymerase chain reaction (PCR). Treatment with cyclohexenonic long-chain fatty alcohol did not alter the diabetic status of the GK rats, i.e., body weight, serum glucose, and serum insulin levels, but significantly ameliorated diabetes-induced hypercontractility of the rat ileum caused by carbachol in a dose-dependent manner. Although there were no significant differences in the expression levels of muscarinic M(3) receptor mRNAs in any of the groups, cyclohexenonic long-chain fatty alcohol reversed the diabetes-induced up-regulation of intestinal muscarinic M(2) receptor mRNAs in treatment groups. These results indicate that cyclohexenonic long-chain fatty alcohol exerts its therapeutic effects on hypercontractility in the ileum of 70-week-old GK type 2 diabetic rats by ameliorating overexpression of muscarinic M(2) receptors.

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Section: Discussionmentioning

confidence: 69%

Characterization of the ileal muscarinic receptor system in 70-week-old type II Goto–Kakizaki diabetic rats; effects of cyclohexenonic long-chain fatty alcohol

Okada¹,

Saito²,

Kinoshita³

et al. 2009

European Journal of Pharmacology

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“…= −0.85, −0.32; p < 0.001; I 2 = 75.09%; based on 70 comparisons from 14 studies [ 32 , 37 , 38 , 41 , 42 , 44 – 47 , 89 – 93 ]) and an increase in hypoinsulinemic (Hedges’ g = 1.37, 95%C.I. = 0.45, 2.29; p = 0.004; I 2 = 83.60%; based on 12 comparisons from six studies [ 94 – 99 ]) and insulin-resistant animals (Hedges’ g = 0.34, 95% C.I. = 0.02, 0.66; p = 0.04; I 2 = 0%; based on two studies [ 57 , 100 ] providing eight comparisons).…”

Section: Resultsmentioning

confidence: 99%

“…5, hyperinsulinemic animals showed lower glutamic acid decarboxylase (GAD) mRNA (Hedges'g = −6.35; 95% [32,37,38,41,42,[44][45][46][47][89][90][91][92][93]) and an increase in hypoinsulinemic (Hedges' g = 1.37, 95%C.I. = 0.45, 2.29; p = 0.004; I 2 = 83.60%; based on 12 comparisons from six studies [94][95][96][97][98][99]) and insulin-resistant animals (Hedges'g = 0.34, 95% C.I. = 0.02, 0.66; p = 0.04; I 2 = 0%; based on two studies [57,100] providing eight comparisons).…”

Section: Gabaergic Outcomesmentioning

confidence: 99%

Insulin effects on core neurotransmitter pathways involved in schizophrenia neurobiology: a meta-analysis of preclinical studies. Implications for the treatment

et al. 2023

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Impairment of insulin action and metabolic dysregulation have traditionally been associated with schizophrenia, although the molecular basis of such association remains still elusive. The present meta-analysis aims to assess the impact of insulin action manipulations (i.e., hyperinsulinemia, hypoinsulinemia, systemic or brain insulin resistance) on glutamatergic, dopaminergic, γ-aminobutyric acid (GABA)ergic, and serotonergic pathways in the central nervous system. More than one hundred outcomes, including transcript or protein levels, kinetic parameters, and other components of the neurotransmitter pathways, were collected from cultured cells, animals, or humans, and meta-analyzed by applying a random-effects model and adopting Hedges’g to compare means. Two hundred fifteen studies met the inclusion criteria, of which 180 entered the quantitative synthesis. Significant impairments in key regulators of synaptic plasticity processes were detected as the result of insulin handlings. Specifically, protein levels of N-methyl-D-aspartate receptor (NMDAR) subunits including type 2A (NR2A) (Hedges’ g = −0.95, 95%C.I. = −1.50, −0.39; p = 0.001; I2 = 47.46%) and 2B (NR2B) (Hedges’g = −0.69, 95%C.I. = −1.35, −0.02; p = 0.043; I2 = 62.09%), and Postsynaptic density protein 95 (PSD-95) (Hedges’g = −0.91, 95%C.I. = −1.51, −0.32; p = 0.003; I2 = 77.81%) were found reduced in insulin-resistant animal models. Moreover, insulin-resistant animals showed significantly impaired dopamine transporter activity, whereas the dopamine D2 receptor mRNA expression (Hedges’g = 3.259; 95%C.I. = 0.497, 6.020; p = 0.021; I2 = 90.61%) increased under insulin deficiency conditions. Insulin action modulated glutamate and GABA release, as well as several enzymes involved in GABA and serotonin synthesis. These results suggest that brain neurotransmitter systems are susceptible to insulin signaling abnormalities, resembling the discrete psychotic disorders’ neurobiology and possibly contributing to the development of neurobiological hallmarks of treatment-resistant schizophrenia.

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“…Diabetes mellitus (DM) is characterized by hyperglycemia resulting from defective or deficient insulin response, and associated with complications affecting many organs, such as the eyes, kidneys, heart, blood vessels and nervous system [1][2][3][4]. The Zucker diabetic fatty (ZDF) rat, a model of type 2 diabetes, accounts for more than 90% of the diabetic population.…”

Section: Introductionmentioning

confidence: 99%

Metformin Normalizes Type 2 Diabetes-Induced Decrease in Cell Proliferation and Neuroblast Differentiation in the Rat Dentate Gyrus

et al. 2010

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In this study, we observed the effects of metformin, one of the most widely prescribed drugs for the treatment of type 2 diabetes, on cell proliferation and neuroblast differentiation in the subgranular zone of the hippocampal dentate gyrus (SZDG) in Zucker diabetic fatty (ZDF) rats, which are a model for type 2 diabetes. For this, metformin was administered orally once a day to 14-week-old ZDF rats for 2 weeks and the animals were sacrificed at 16 weeks of age. During this period, blood glucose levels were higher in the vehicle-treated ZDF rats than in the Zucker lean control (ZLC) rats. Metformin treatment significantly decreased the blood glucose levels from 15.5 weeks of age. In the SZDG, Ki67 (a marker for cell proliferation)- and doublecortin (DCX, a marker for differentiated neuroblasts)-immunoreactive cells were much lower in the vehicle-treated ZDF rats than in the ZLC rats. In the metformin-treated ZDF group, Ki67- and DCX-immunoreactive cells were significantly increased in the SZDG compared to those in the vehicle-treated ZDF group. These results suggest that diabetes significantly reduces cell proliferation and neuroblast differentiation in the SZDG and that metformin treatment normalizes the reduction of cell proliferation and neuroblast differentiation in the SZDG in diabetic rats.

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Effects of Cyclohexanonic Long-Chain Fatty Alcohol, tCFA15 on Amino Acids in Diabetic Rat Brain: A Preliminary Study

Cited by 4 publications

References 57 publications

Characterization of the ileal muscarinic receptor system in 70-week-old type II Goto–Kakizaki diabetic rats; effects of cyclohexenonic long-chain fatty alcohol

Characterization of the ileal muscarinic receptor system in 70-week-old type II Goto–Kakizaki diabetic rats; effects of cyclohexenonic long-chain fatty alcohol

Insulin effects on core neurotransmitter pathways involved in schizophrenia neurobiology: a meta-analysis of preclinical studies. Implications for the treatment

Metformin Normalizes Type 2 Diabetes-Induced Decrease in Cell Proliferation and Neuroblast Differentiation in the Rat Dentate Gyrus

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