Rosiglitazone attenuates the cognitive deficits induced by high fat diet feeding in rats

Pathan, Asif R.; Gaikwad, Anil Bhanudas; Viswanad, Bhoomi; Ramarao, P.

doi:10.1016/j.ejphar.2008.06.016

Cited by 93 publications

(40 citation statements)

References 27 publications

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“…In rats, rosiglitazone not only reduced the adverse metabolic effects of a high-fat diet, but also its memory-impairing impact [50]. It is tempting to speculate that the mechanisms underlying these observations derive at least in part from an enhancing influence of rosiglitazone on central nervous insulin sensitivity.…”

Section: Therapeutic Perspectivesmentioning

confidence: 94%

Central nervous insulin resistance: a promising target in the treatment of metabolic and cognitive disorders?

Hallschmid

Schultes

2009

Diabetologia

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Research on functions and signalling pathways of insulin has traditionally focused on peripheral tissues such as muscle, fat and liver, while the brain was commonly believed to be insensitive to the effects of this hormone secreted by pancreatic beta cells. However, since the discovery some 30 years ago that insulin receptors are ubiquitously found in the central nervous system, an evergrowing research effort has conclusively shown that circulating insulin accesses the brain, which itself does not synthesise insulin, and exerts pivotal functions in central nervous networks. As an adiposity signal reflecting the amount of body fat, insulin provides direct negative feedback to hypothalamic nuclei that control whole-body energy and glucose homeostasis. Moreover, insulin affects distinct cognitive processes, e.g. by triggering the formation of psychological memory contents. Accordingly, metabolic and cognitive disorders such as obesity, type 2 diabetes mellitus and Alzheimer's disease are associated with resistance of central nervous structures to the effects of insulin, which may derive from genetic polymorphisms as well as from long-term exposure to excess amounts of circulating insulin due to peripheral insulin resistance. Thus, overcoming central nervous insulin resistance, e.g. by pharmacological interventions, appears to be an attractive strategy in the treatment and prevention of these disorders. Enhancement of central nervous insulin signalling by administration of intranasal insulin, insulin analogues and insulin sensitisers in basic research approaches has yielded encouraging results that bode well for the successful translation of these effects into future clinical practice.

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Section: Therapeutic Perspectivesmentioning

confidence: 94%

Central nervous insulin resistance: a promising target in the treatment of metabolic and cognitive disorders?

Hallschmid

Schultes

2009

Diabetologia

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“…It has also been suggested that brain insulin receptor signaling is markedly reduced in AD brain (Frolich et al 1999;Messier and Teutenberg 2005). Further reports illustrate that increasing plasma insulin levels in patients with insulin resistance causes a concurrent increase in brain levels of amyloid-beta and inflammatory markers (Craft et al 2003, Craft 2006Pathan et al 2008). Amyloid build up during hyperinsulinemia may arise as an outcome of reduced Aβ degradation by insulin-degrading enzyme (IDE) (Farris et al 2004(Farris et al , 2005.…”

Section: Insulin Sensitivitymentioning

confidence: 95%

Neuroprotective mechanisms of peroxisome proliferator-activated receptor agonists in Alzheimer’s disease

Sodhi

Singh

Jaggi

2011

Naunyn-Schmiedeberg's Arch Pharmacol

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Alzheimer's disease (AD) is the most common causes of dementia accounting for 50-60% of all cases. The pathological hallmarks of AD are the formation of extracellular plaques consisting of amyloid-β protein, intracellular neurofibrillary tangles of hyperphosphorylated tau proteins and presence of chronic neuroinflammation causing progressive decline in memory and cognitive functions. The current therapeutic strategies to improve memory deficits aim at preventing the formation and accumulation of amyloid-β and tau phosphorylation. Beyond the plaque and tangle-related targets, other aspects of pathophysiology including molecular transport mechanism, oxidative damage, inflammation and glucose and lipid metabolism may also provide opportunities to slow down the progression of memory loss. A novel therapeutic approach to the treatment of AD is through the exploration of nuclear receptor agonists, peroxisome proliferator-activated receptors (PPARs), which have been clinically used as antidiabetic and dyslipidemic agents. The findings that PPAR agonists may possess antiamyloidogenic, anti-inflammatory, insulin-sensitizing, and cholesterol-lowering potential suggest that they could be interesting candidates for AD drugs. Through this review, we will discuss the probable pathophysiological mechanisms that may elicit the defending role of these receptors in brains of AD patients.

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“…It facilitates insulin's action for the treatment of type 2 diabetes and prevents cognitive decline and ischemic brain injury (Kumar et al 2009;Shimazu et al 2005;Sundararajan et al 2005). Some latest studies reported that PPAR-γ agonists, thiazolidinediones modulated Ca 2+ -dependent pathways in hippocampal cultured neurons (Pancani et al 2009), overcame the cognitive deficits arising from high fat diet feeding, which may be in part mediated through the development of peripheral insulin resistance (Pathan et al 2008). Moreover, PPAR-γ agonist, darglitazone restores acute inflammatory responses to cerebral hypoxiaischemia in the diabetic mouse (Kumari et al 2010).…”

Section: Malementioning

confidence: 98%

Female exhibited severe cognitive impairment in type 2 diabetes mellitus mice

et al. 2010

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Rosiglitazone attenuates the cognitive deficits induced by high fat diet feeding in rats

Cited by 93 publications

References 27 publications

Central nervous insulin resistance: a promising target in the treatment of metabolic and cognitive disorders?

Central nervous insulin resistance: a promising target in the treatment of metabolic and cognitive disorders?

Neuroprotective mechanisms of peroxisome proliferator-activated receptor agonists in Alzheimer’s disease

Female exhibited severe cognitive impairment in type 2 diabetes mellitus mice

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