Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Metabolic syndrome is associated with insulin resistance and atherosclerosis. Here, we show that deficiency of one or two alleles of ATM, the protein mutated in the cancer-prone disease ataxia telangiectasia, worsens features of the metabolic syndrome, increases insulin resistance, and accelerates atherosclerosis in apoE-/- mice. Transplantation with ATM-/- as compared to ATM+/+ bone marrow increased vascular disease. Jun N-terminal kinase (JNK) activity was increased in ATM-deficient cells. Treatment of ATM+/+apoE-/- mice with low-dose chloroquine, an ATM activator, decreased atherosclerosis. In an ATM-dependent manner, chloroquine decreased macrophage JNK activity, decreased macrophage lipoprotein lipase activity (a proatherogenic consequence of JNK activation), decreased blood pressure, and improved glucose tolerance. Chloroquine also improved metabolic abnormalities in ob/ob and db/db mice. These results suggest that ATM-dependent stress pathways mediate susceptibility to the metabolic syndrome and that chloroquine or related agents promoting ATM activity could modulate insulin resistance and decrease vascular disease.
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PMID:ATM-dependent suppression of stress signaling reduces vascular disease in metabolic syndrome. 1708 7

Erectile dysfunction is an important cause of decreased quality of life in men. It is estimated that approximately 30 million men in the US and 100 million worldwide may have erectile dysfunction. Data from epidemiological studies indicate a higher prevalence of impotence in obese men. Obesity may be a risk factor for sexual dysfunction in both sexes; data for the metabolic syndrome are very preliminary and need to be confirmed in larger epidemiological studies. The high prevalence of erectile dysfunction in patients with cardiovascular risk factors suggests that abnormalities of the vasodilator system of penile arteries play an important role in the pathophysiology of erectile dysfunction. Nitric oxide released during non-adrenergic, non-cholinergic neurotransmission and from the endothelium is probably the principal neurotransmitter mediating penile erection. It has been shown that chloroquine administration was associated with an increase in nitric oxide synthesis. Chloroquine was also postulated to enhance insulin sensitivity, which suggests potential benefit in treating the metabolic syndrome-related erectile dysfunction.
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PMID:Chloroquine-induced nitric oxide as a potential treatment of erectile dysfunction associated with the metabolic syndrome: the science and the fiction. 1760 95