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Impact of Nutrition on Cerebral Circulation and Cognition in the Metabolic Syndrome.

Mellendijk L, Wiesmann M, Kiliaan AJ - Nutrients (2015)

Bottom Line: Not only does the peripheral vasculature seem to be affected, but the syndrome has a profound impact on the cerebral circulation and thence brain structure as well.Furthermore, strong associations are shown with stroke, cognitive impairment, and dementia.In this review the impact of nutrition on the individual components of MetS, the effects of MetS on peripheral and cerebral vasculature, and its consequences for brain structure and function will be discussed.

View Article: PubMed Central - PubMed

Affiliation: Department of Anatomy, Radboud University Medical Center, Donders Institute for Brain, Cognition and Behaviour, Nijmegen 6500 HB, The Netherlands. mellendijklaura@gmail.com.

ABSTRACT
The increasing prevalence of Metabolic Syndrome (MetS), defined as the clustering of abdominal obesity, dyslipidemia, hypertension, and hyperglycemia, appears to be driving the global epidemics cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM). Nutrition has a major impact on MetS and plays an important role in the prevention, development, and treatment of its features. Structural and functional alterations in the vasculature, associated with MetS, might form the link between MetS and the increased risk of developing CVD and T2DM. Not only does the peripheral vasculature seem to be affected, but the syndrome has a profound impact on the cerebral circulation and thence brain structure as well. Furthermore, strong associations are shown with stroke, cognitive impairment, and dementia. In this review the impact of nutrition on the individual components of MetS, the effects of MetS on peripheral and cerebral vasculature, and its consequences for brain structure and function will be discussed.

No MeSH data available.


Related in: MedlinePlus

(a) The four components abdominal obesity, dyslipidemia, hypertension, and hyperglycemia comprising Metabolic Syndrome (MetS), contribute all to structural and functional alterations in the peripheral and brain vasculature. Associated factors highly contributing to the development of MetS are inappropriate diets physical inactivity, advancing age, and various hormones (not depicted here). Abdominal obesity is associated with metabolic alterations, including elevated FFA’s and an altered production of proinflammatory and anti-inflammatory adipokines resulting in a pro-inflammatory status. Atherogenic dyslipidemia involves hypertriglyceridemia, decreased levels of HDL-C, increased VLDL and interaction with RAAS. Increased RAAS activity is one of the mechanisms causing elevated blood pressure levels. Hypertension contributes to the atherosclerotic process and increased vascular stiffening and remodeling. Hyperglycemia is often proceeded and accompanied by IR and both influence the atherosclerotic process. Several associations and interactions are found within these processes and are also related to IR and T2DM. Alterations in the vasculature might lead to an increased vascular resistance, pro-thrombotic status, stroke, and microbleeds, while reductions are found in capillary density, cerebral autoregulation, and CBF. These features can accelerate the development of WML and cerebral atrophy, which eventually increase the risk of developing MCI and dementia. FFA = free fatty acids, HDL-C = high density lipoprotein cholesterol, VLDL = very-low-density lipoprotein, RAAS = renin-angiotensin-aldosterone-system, IR = insulin resistance, T2DM = type 2 diabetes mellitus, CBF = cerebral blood flow, WML = white matter lesions, MCI = mild cognitive impairment; (b) Scheme of the potential influence of dietary components on MetS and related impairment of cerebral vasculature and cognition [148,149,151,189].
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nutrients-07-05477-f001: (a) The four components abdominal obesity, dyslipidemia, hypertension, and hyperglycemia comprising Metabolic Syndrome (MetS), contribute all to structural and functional alterations in the peripheral and brain vasculature. Associated factors highly contributing to the development of MetS are inappropriate diets physical inactivity, advancing age, and various hormones (not depicted here). Abdominal obesity is associated with metabolic alterations, including elevated FFA’s and an altered production of proinflammatory and anti-inflammatory adipokines resulting in a pro-inflammatory status. Atherogenic dyslipidemia involves hypertriglyceridemia, decreased levels of HDL-C, increased VLDL and interaction with RAAS. Increased RAAS activity is one of the mechanisms causing elevated blood pressure levels. Hypertension contributes to the atherosclerotic process and increased vascular stiffening and remodeling. Hyperglycemia is often proceeded and accompanied by IR and both influence the atherosclerotic process. Several associations and interactions are found within these processes and are also related to IR and T2DM. Alterations in the vasculature might lead to an increased vascular resistance, pro-thrombotic status, stroke, and microbleeds, while reductions are found in capillary density, cerebral autoregulation, and CBF. These features can accelerate the development of WML and cerebral atrophy, which eventually increase the risk of developing MCI and dementia. FFA = free fatty acids, HDL-C = high density lipoprotein cholesterol, VLDL = very-low-density lipoprotein, RAAS = renin-angiotensin-aldosterone-system, IR = insulin resistance, T2DM = type 2 diabetes mellitus, CBF = cerebral blood flow, WML = white matter lesions, MCI = mild cognitive impairment; (b) Scheme of the potential influence of dietary components on MetS and related impairment of cerebral vasculature and cognition [148,149,151,189].

Mentions: The concept of MetS has been mainly associated with the peripheral systems and in this review we broadened this concept with respect to the brain, its cerebral circulation, and the impact on cognition. An overview is given in Figure 1a. MetS and its features not only affect the peripheral vasculature, but also induce structural and functional alterations in the cerebral vasculature, including resistance, stiffening, and remodeling. This seems to affect the brain in multiple ways. For instance, changes in the cerebral microcirculation can affect larger vessels and CBF. Changes in cerebral microcirculation also contribute to the development of cerebral small vessel disease possibly leading to white matter lesions (WML), changes in gray matter microstructure, cerebral microbleeds, and brain cell (neuronal) atrophy. The affected brain tissue integrity might be a consequence of brain perfusion alterations, cerebral autoregulation disturbances, vascular reactivity abnormalities, or an altered production and secretion of peripheral adipokines including some oligomers of adiponectin, leptin, TNF-α, and IL-6. Leptin, TNF-α, and IL-6 are all able to cross the BBB and exert a wide range of effects on brain functioning. Eventually, all these factors together may lead to an increased risk of developing MCI, dementia, and stroke.


Impact of Nutrition on Cerebral Circulation and Cognition in the Metabolic Syndrome.

Mellendijk L, Wiesmann M, Kiliaan AJ - Nutrients (2015)

(a) The four components abdominal obesity, dyslipidemia, hypertension, and hyperglycemia comprising Metabolic Syndrome (MetS), contribute all to structural and functional alterations in the peripheral and brain vasculature. Associated factors highly contributing to the development of MetS are inappropriate diets physical inactivity, advancing age, and various hormones (not depicted here). Abdominal obesity is associated with metabolic alterations, including elevated FFA’s and an altered production of proinflammatory and anti-inflammatory adipokines resulting in a pro-inflammatory status. Atherogenic dyslipidemia involves hypertriglyceridemia, decreased levels of HDL-C, increased VLDL and interaction with RAAS. Increased RAAS activity is one of the mechanisms causing elevated blood pressure levels. Hypertension contributes to the atherosclerotic process and increased vascular stiffening and remodeling. Hyperglycemia is often proceeded and accompanied by IR and both influence the atherosclerotic process. Several associations and interactions are found within these processes and are also related to IR and T2DM. Alterations in the vasculature might lead to an increased vascular resistance, pro-thrombotic status, stroke, and microbleeds, while reductions are found in capillary density, cerebral autoregulation, and CBF. These features can accelerate the development of WML and cerebral atrophy, which eventually increase the risk of developing MCI and dementia. FFA = free fatty acids, HDL-C = high density lipoprotein cholesterol, VLDL = very-low-density lipoprotein, RAAS = renin-angiotensin-aldosterone-system, IR = insulin resistance, T2DM = type 2 diabetes mellitus, CBF = cerebral blood flow, WML = white matter lesions, MCI = mild cognitive impairment; (b) Scheme of the potential influence of dietary components on MetS and related impairment of cerebral vasculature and cognition [148,149,151,189].
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4663605&req=5

nutrients-07-05477-f001: (a) The four components abdominal obesity, dyslipidemia, hypertension, and hyperglycemia comprising Metabolic Syndrome (MetS), contribute all to structural and functional alterations in the peripheral and brain vasculature. Associated factors highly contributing to the development of MetS are inappropriate diets physical inactivity, advancing age, and various hormones (not depicted here). Abdominal obesity is associated with metabolic alterations, including elevated FFA’s and an altered production of proinflammatory and anti-inflammatory adipokines resulting in a pro-inflammatory status. Atherogenic dyslipidemia involves hypertriglyceridemia, decreased levels of HDL-C, increased VLDL and interaction with RAAS. Increased RAAS activity is one of the mechanisms causing elevated blood pressure levels. Hypertension contributes to the atherosclerotic process and increased vascular stiffening and remodeling. Hyperglycemia is often proceeded and accompanied by IR and both influence the atherosclerotic process. Several associations and interactions are found within these processes and are also related to IR and T2DM. Alterations in the vasculature might lead to an increased vascular resistance, pro-thrombotic status, stroke, and microbleeds, while reductions are found in capillary density, cerebral autoregulation, and CBF. These features can accelerate the development of WML and cerebral atrophy, which eventually increase the risk of developing MCI and dementia. FFA = free fatty acids, HDL-C = high density lipoprotein cholesterol, VLDL = very-low-density lipoprotein, RAAS = renin-angiotensin-aldosterone-system, IR = insulin resistance, T2DM = type 2 diabetes mellitus, CBF = cerebral blood flow, WML = white matter lesions, MCI = mild cognitive impairment; (b) Scheme of the potential influence of dietary components on MetS and related impairment of cerebral vasculature and cognition [148,149,151,189].
Mentions: The concept of MetS has been mainly associated with the peripheral systems and in this review we broadened this concept with respect to the brain, its cerebral circulation, and the impact on cognition. An overview is given in Figure 1a. MetS and its features not only affect the peripheral vasculature, but also induce structural and functional alterations in the cerebral vasculature, including resistance, stiffening, and remodeling. This seems to affect the brain in multiple ways. For instance, changes in the cerebral microcirculation can affect larger vessels and CBF. Changes in cerebral microcirculation also contribute to the development of cerebral small vessel disease possibly leading to white matter lesions (WML), changes in gray matter microstructure, cerebral microbleeds, and brain cell (neuronal) atrophy. The affected brain tissue integrity might be a consequence of brain perfusion alterations, cerebral autoregulation disturbances, vascular reactivity abnormalities, or an altered production and secretion of peripheral adipokines including some oligomers of adiponectin, leptin, TNF-α, and IL-6. Leptin, TNF-α, and IL-6 are all able to cross the BBB and exert a wide range of effects on brain functioning. Eventually, all these factors together may lead to an increased risk of developing MCI, dementia, and stroke.

Bottom Line: Not only does the peripheral vasculature seem to be affected, but the syndrome has a profound impact on the cerebral circulation and thence brain structure as well.Furthermore, strong associations are shown with stroke, cognitive impairment, and dementia.In this review the impact of nutrition on the individual components of MetS, the effects of MetS on peripheral and cerebral vasculature, and its consequences for brain structure and function will be discussed.

View Article: PubMed Central - PubMed

Affiliation: Department of Anatomy, Radboud University Medical Center, Donders Institute for Brain, Cognition and Behaviour, Nijmegen 6500 HB, The Netherlands. mellendijklaura@gmail.com.

ABSTRACT
The increasing prevalence of Metabolic Syndrome (MetS), defined as the clustering of abdominal obesity, dyslipidemia, hypertension, and hyperglycemia, appears to be driving the global epidemics cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM). Nutrition has a major impact on MetS and plays an important role in the prevention, development, and treatment of its features. Structural and functional alterations in the vasculature, associated with MetS, might form the link between MetS and the increased risk of developing CVD and T2DM. Not only does the peripheral vasculature seem to be affected, but the syndrome has a profound impact on the cerebral circulation and thence brain structure as well. Furthermore, strong associations are shown with stroke, cognitive impairment, and dementia. In this review the impact of nutrition on the individual components of MetS, the effects of MetS on peripheral and cerebral vasculature, and its consequences for brain structure and function will be discussed.

No MeSH data available.


Related in: MedlinePlus