4 research outputs found
Metabolic syndrome and risk of major coronary events among the urban diabetic patients: North Indian Diabetes and Cardiovascular Disease Study-NIDCVD-2
Objective: The present study aimed at estimating the prevalence of metabolic syndrome (MetS) and prospectively, evaluating cardiovascular events among Asian Indians type 2 diabetic subjects. Methods: The sample comprised 1522 type 2 diabetic mellitus (T2DM) subjects aged 25-91. years, who participated in the North Indian Diabetes and Cardiovascular Disease Study (NIDCVD). The participants were screened for hypertension, dyslipidemia, obesity and cardiovascular events. Anthropometric, clinical and biochemical measurements were done in all subjects. The prevalence of MetS was estimated in all the subjects according to the harmonized criteria of 2009. Results: The prevalence of MetS among urban Indian diabetic subjects was 71.9% and was significantly higher in females (86%) as compared to males (57.9%). To determine the independent predictors of the MetS in diabetic sample, binary logistic regression analyses were performed using demographic and biochemical parameters. Significant differences in the indices of generalized and abdominal obesity and lipids (total cholesterol, high density lipoprotein) were observed (p <. 0.01) in male:female and MetS and non-MetS comparisons. Regression analysis for prediction of CAD showed that family history, age, body mass index (BMI), SBP, physical inactivity and hypertension independently and significantly predicted the disease outcome. Binary logistic regression analysis revealed that MetS may be an independent risk/predictor of CAD (odd ratio (OR) = 3.44, CI 1.31-9.01, p = 0.012) along with higher age groups, BMI and hypertension in Indian population. Conclusion: The study demonstrated that the high prevalence of MetS and its different components were positively associated with a higher risk of CAD in north Indian diabetic subjects. Nevertheless, MetS is a major health problem in India, comprehensive population studies are warranted for estimation of incidence and prevalence, and education should be provided on its prevention and control to reduce the diabetes-related morbidity and mortality
Paraoxonase 1 gene polymorphisms (Q192R and L55M) are associated with coronary artery disease susceptibility in Asian Indians
Background: Coronary artery disease (CAD) is a complex
metabolic disorder in which lifestyle and genetic factors are
known to play key roles in pathogenesis. The paraoxonase 1
(PON1) enzyme has a defensive effect against CAD progression,
as it safeguards low-density lipoproteins (LDLs) from
oxidative modifications. The most extensively studied genetic
variants in the PON1 gene are Q192R and L55M, which
have been related with LDL antioxidative activity and risk of
CAD. Objective: The present case-control study intended to
examine the Q192R and L55M polymorphisms and their association
with the risk of CAD patients in north Indians.
Methods: A total of 872 subjects (412 CAD patients and 460
controls) were recruited from north India. The PON1 gene
was amplified and genotypes were studies using PCR-RFLP.
χ2 analysis was performed to compare genotype/allele frequencies
in patients and controls. Results: The present study indicated abdominal obesity, elevated body mass index, and
dyslipidemia with increased levels of total cholesterol and
triglycerides as well as reduced high-density lipoprotein
cholesterol in CAD subjects compared to healthy controls
(p < 0.05). Logistic regression analysis of the data revealed an
association of the RR genotype of the Q192R polymorphism
with an about 2-fold elevated risk of CAD (OR = 2.23, 95%
CI = 1.47–3.37, p = 0.0001). Contrariwise, the L55M polymorphism
did not show significant association with CAD (OR =
1.81, 95% CI = 0.66–4.95, p = 0.326). Conclusions: The Q192R
polymorphism in the PON1 gene may be a susceptibility
gene associated with increased risk of CAD in an Asian Indian
population
ENPP1 K121Q functional variant enhances susceptibility to insulin resistance and dyslipidemia with metabolic syndrome in Asian Indians
Background: Ectonucleotide pyrophosphatase/phosphodiesterase1
(ENPP1/PC-1) is a key modulator of the insulin signaling
pathway, and its common variant, K121Q, increases
the susceptibility to diabetes and cardiovascular diseases.
Objectives: The main objective of the present study was to
investigate the association of ENPP1 K121Q polymorphism
with the pathophysiology of metabolic syndrome (MetS) in
a north Indian population. Methods: A total of 567 participants
(303 MetS subjects and 264 healthy controls) were examined
for ENPP1 genotypes and various clinical parameters,
including body mass index (BMI), waist circumference
(WC), systolic and diastolic blood pressures (SBP/DBP), fasting
blood glucose (FBG), cholesterol, triglycerides (TG), highdensity
lipoprotein, and insulin. Genotyping was performed
using polymerase chain reaction-restriction fragment length
polymorphism (PCR-RFLP). Statistical analysis of the data
was done using SPSS. Results: Significant increases in BMI,
WC, SBP, DBP, FBG, TG, low-density lipoprotein, insulin, and
Homeostasis Model Assessment of insulin resistance (HOMAIR)
and of beta-cell function (HOMA-BF) were observed in
MetS patients compared to healthy controls. Logistic regression
analysis of data demonstrated a nonsignificant association
of QQ and KQ+QQ genotypes with increased risk of
MetS (OR [95% CI], 1.583 [0.455–5.507], p = 0.470 for QQ genotypes
and 1.097 [0.784–1.540], p = 0.587 for KQ+QQ genotypes).
Moreover, MetS subjects carrying Q alleles had significantly
higher levels of TG, insulin, body fat percentage,
and insulin resistance as evident by higher values of HOMAIR.
Conclusions: We conclude that ENPP1 K121Q functional
variant enhances susceptibility to insulin resistance and dyslipidemia
in MetS subjects of an Asian Indian population
Targeting mitochondrial bioenergetics as a promising therapeutic strategy in metabolic and neurodegenerative diseases
Mitochondria are the organelles that generate energy for the cells and act as biosynthetic and bioenergetic factories, vital for normal cell functioning and human health. Mitochondrial bioenergetics is considered an important measure to assess the pathogenesis of various diseases. Dysfunctional mitochondria affect or cause several conditions involving the most energy-intensive organs, including the brain, muscles, heart, and liver. This dysfunction may be attributed to an alteration in mitochondrial enzymes, increased oxidative stress, impairment of electron transport chain and oxidative phosphorylation, or mutations in mitochondrial DNA that leads to the pathophysiology of various pathological conditions, including neurological and metabolic disorders. The drugs or compounds targeting mitochondria are considered more effective and safer for treating these diseases. In this review, we make an effort to concise the available literature on mitochondrial bioenergetics in various conditions and the therapeutic potential of various drugs/compounds targeting mitochondrial bioenergetics in metabolic and neurodegenerative diseases.</p