A new study supports the beneficiary role of pharmaco-genetic interventions in patients with metabolic syndrome.
Metabolic syndrome may well be described as the super villain of the modern era. This evil evolves when an erratic life style backfires. Metabolic syndrome or syndrome X is characterized by resistance to the hormone insulin, abdominal obesity, high blood pressure and cholesterol abnormalities. A combination of these risk factors places an individual at an increased risk for heart disease, stroke, and type 2 diabetes.
AdvertisementBlood pressure strongly correlates with body mass index (BMI, body weight divided by the square of height) and is a major determinant of heart's function. Obesity exerts a deleterious effect on the heart through a number of mechanisms, some of which are independent of hypertension.
Among the multitude of features of the modern lifestyle responsible for syndrome X, high fat diet stands out. High dietary fat intake is a major risk factor for the disruption of cardiovascular and metabolic function. A recent study examined the effect of high fat (HF) diet on the structure and function of heart and blood vessels in spontaneously hypertensive rats (SHR). SHR were fed a high fat diet for 15 weeks. Body weight, total cholesterol and blood pressure levels were monitored. The values of these parameters confirmed the development of a metabolic syndrome like makeup in SHRs. An accelerated decline in heart function was noticed in SHRs fed on high fat diet.
The current study also looked into one of the chief underlying pathological mechanisms of metabolic syndrome called oxidative stress. This refers to the body's inability to detoxify reactive oxygen species. Significant damage is produced by oxidative stress. The human body has a defense mechanism called heme-heme oxidase (heme-HO) system to combat this stress. Adiponectin is another protective agent. Adiponectin, a protein secreted by fat cells (adipocytes), regulates the metabolism of lipids and glucose. High blood levels of adiponectin are known to be protective against heart failure. Obese people have low levels of this protein.
Increased expression of the gene regulating the enzyme heme oxygenase-1, which also increases levels of adiponectin, was found to prevent dysfunction of heart and blood vessels in SHRs fed a high fat diet. This result encourages the development of treatment strategies that enhance HO-1 expression.
Pharmaco-genetic interventions that target HO-1-adiponectin axis may have a beneficiary role in patients with metabolic syndrome. Lifestyle modification, however, continues to be the preferred treatment of metabolic syndrome. Altered diet and exercise that lead to weight reduction are protective against the condition.
Reference: High fat diet enhances cardiac abnormalities in SHR rats: Protective role of heme oxygenase-adiponectin axis; Jian et al; BMC Diabetology & Metabolic syndrome.
PInsults in Mother’s Womb and During First Month After Birth Can Cause Long-Term Neurological Defects in Children Aberrant Connectivity Between Key Regions of the Brain Responsible for Major Depressive Disorder M