The Metabolic Syndrome: Epidemiology Clinical Treatment and Underlying Mechanisms

Metabolic syndrome and cognitive impairment
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Contents:

  • Review ARTICLE
  • Metabolic syndrome in HIV-infected individuals: underlying mechanisms and epidemiological aspects
  • A Comprehensive Review on Metabolic Syndrome

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    Some drugs may prevent or inhibit AGEs formation and accumulation. Studies on this compound, however, have been discontinued due to its toxicity Yan et al. Recovery consisted of a reduction in microglial and macrophage activation, a decreased rate of apoptosis, and an improved neurobehavioral function Ding et al.

    As already mentioned, one of our research lines investigates the effects of chronic cola beverages consumption in murine models.

    Review ARTICLE

    Clear evidence of beneficial effects of a wash-out period diet and exercise have been reported Milei et al. Another study conducted in our institution included elderly patients of both sexes that attended periodical routine check-ups, with the purpose of evaluating the effectiveness of short-term antioxidant supplementation. The outcome of our study confirmed that antioxidant supplementation improved plasma biochemistry as a result of changes in oxidative metabolism, typically in those patients having low basal endogenous antioxidants concentration in plasma.

    Based on these results, we recommended measuring the basal level of plasma antioxidants before starting any supplementation with antioxidants in elderly cardiovascular patients, a particularly vulnerable population with special precautions to be endorsed. Using an experimental model, we assessed the therapeutic benefits of medical grade ozone, a mixture of 0. We reported promising effects of medical ozone auto-hemotransfusion on the cardiovascular system injury.

    Metabolic syndrome in HIV-infected individuals: underlying mechanisms and epidemiological aspects

    Pretreatment with ozone auto-hemotransfusion decreased neointimal proliferation and induced reendothelialization following a metal stent insertion Barone et al. The protective mechanism whereby ozone reduces restenosis appears to involve the ozone well-described oxidative preconditioning upregulating the antioxidant enzymes, and improving the antioxidant response to an eventual injury Barone et al. Cognitive impairment or skills were not assessed in these experimental models.

    However, the promising outcome encourages pursuing further study of cognitive abilities as well. Among neurodegenerative disorders, AD has been extensively studied regarding cognitive impairment in the setting of MetS Hashimoto et al. This tendency is reasonable since there is genetic evidence showing the apolipoprotein E ApoE as a common gene which links dementia, MetS, and diabetes Zhang et al. Moreover, it is also crucial to bear in mind the extent of hardships that come hand in hand with AD i. One of the challenges for public health is to identify risk factors, and the MetS is definitely a prevailing one.

    The compelling association between altered metabolic states and dementia may provide insight on a therapeutic approach that can delay cognitive impairment, targeting the underlying pathophysiological pathways of MetS de la Monte, Staggering evidence demonstrates that AD pathogenesis is strongly associated with oxidative stress, inflammation, and insulin, glucose, and lipid dysregulation; all of these pathological pathways are present in MetS and other altered metabolic states Rojas-Gutierrez et al.

    Consequently, a vast number of studies have shown anti-MetS treatments to improve diverse aspects of cognition in patients with AD Chen et al. An example of said treatments include drugs like gut incretins, thiazolidinediones, and metformin, which show promising results regarding cognitive impairment in animal and clinical trials, improving the effects of insulin via different mechanisms Chen et al. Table 1 summarizes some data observed in clinical trials pertinent to anti-MetS treatment.

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    Furthermore, studies on anti-oxidative treatment in patients with AD also present supportive results. For instance, flavonoids scavenge free radicals and have shown to promote neuronal survival in the hippocampus Venkatesan et al. Another promising antioxidant treatment involves the administration of the synthetic S-acyl derivative of thiamine vitamin B1 Benfotiamine in clinical trials reporting a long-term cognitive improvement, suggesting a possible disease-modifying therapy Pan et al.

    Ultimately, the emerging global epidemic of neurodegenerative disorders as the world population ages is of great concern Brookmeyer et al.

    Any insight regarding neuroprotection and delaying the onset of cognitive impairments is of utmost value. Given these proportions, it has become an epidemic of public health concern. Hyperglycemia, IR, inflammation, oxidative stress, and hypoxia are key pathological pathways associated with MetS. It is a question of time until this cluster of conditions results in tissue damage in target organs such as the brain and the microvasculature that irrigates the nervous system.

    Oxidative stress and hypoxia are actually linked to neurological diseases like Alzheimer's and Parkinson's Kim and Feldman, The therapeutic strategies suggested in this review entail multidisciplinary interventions involving different pathological pathways in concert. These include improving lifestyle and daily habits diet and exercise , treating the cardinal symptoms of MetS, and reducing the pro-oxidative load in affected patients. Antioxidant therapy is not routinely used in MetS, although extensive research relative to its benefits in diabetic neuropathy is available.

    Hence, we consider that diminishing the pro-oxidative status in patients with MetS may play a critical role in reducing brain hypoxic damage and behavioral deficits. NL: Has interpreted the data, revised for intellectual content, approved the final version of the work to be published, and may account for a research work properly accomplished. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

    Accessed October 10, Dementia is the major cause of functional dependence in the elderly: 3-year follow-up data from a population-based study.

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    Public Health 88, — Gut peptides and type 2 diabetes mellitus treatment. Al-Enazi, M.

    A Comprehensive Review on Metabolic Syndrome

    Ameliorative potential of rutin on streptozotocin-induced neuropathic pain in rat. Ametov, A. Diabetes Care 26, — Aoqui, C. Microvascular dysfunction in the course of metabolic syndrome induced by high-fat diet. Arnal, E. Lutein and docosahexaenoic acid prevent cortex lipid peroxidation in streptozotocin-induced diabetic rat cerebral cortex. Neuroscience , — Arts, I.

    What is Metabolic Syndrome? (Syndrome X)

    Polyphenols and disease risk in epidemiologic studies. Baigent, C. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from , participants in 26 randomised trials. Lancet , — Balakumar, P. The multifaceted therapeutic potential of benfotiamine. Baluchnejadmojarad, T. Chronic oral epigallocatechin-gallate alleviates streptozotocin-induced diabetic neuropathic hyperalgesia in rat: involvement of oxidative stress.

    More about research at Mayo Clinic

    PubMed Abstract Google Scholar. Barone, A. Ozonetherapy protects from in-stent coronary neointimal proliferation. Role of redoxins. Bayarsaikhan, E. Microglial AGE-albumin is critical for neuronal death in Parkinson's disease: a possible implication for theranostics. Nanomedicine 10, — Baydas, G. Biochemistry 69, — Beckman, K.

    The free radical theory of aging matures. Belfiore, A. Bhat, A. Oxidative stress, mitochondrial dysfunction and neurodegenerative diseases; a mechanistic insight. Biessels, G. Ageing and diabetes: implications for brain function. Binesh Marvasti, T. Pharmacological management of metabolic syndrome and its lipid complications.

    Daru 18, — Birben, E.