High Prevalence of Abdominal Obesity Increases the Risk of the Metabolic Syndrome in Nigerian Type 2 Diabetes Patients: Using the International Diabetes Federation Worldwide Definition

Ezenwaka, Chidum E.; Okoye, O.; Esonwune, Chibuike; Onuoha, Philip; Dioka, CE; Osuji, CU; Oguejiofor, Celestine Ogonna; Meludu, SC

doi:10.1089/met.2013.0139

Cited by 17 publications

(12 citation statements)

References 42 publications

(67 reference statements)

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“…In contrast to studies in the US, where the prevalence of low HDLC and high TG are similar [69], in studies in Africa, these MetSyn components are often highly discordant. Among Nigerian T2D individuals, 61.8% had low HDLC, while only 10% had low TG [71]. Among Ghanaian hypertension patients with MetSyn, 96% had low HDLC, but only 32% had high TG [72].…”

Section: The Metabolic Syndromementioning

confidence: 99%

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Interethnic Differences in Serum Lipids and Implications for Cardiometabolic Disease Risk in African Ancestry Populations

Bentley¹,

Rotimi

2017

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African Americans are generally found to have a healthier lipid profile (lower triglycerides [TG] and higher high-density lipoprotein cholesterol concentration [HDLC]) compared to those of other ethnicities. Paradoxically, African Americans do not experience a decreased risk of the cardiometabolic diseases that serum lipids are expected to predict. This review explores this mismatch between biomarker and disease among African ancestry individuals by investigating the presence of interethnic differences in the biological relationships underlying the serum lipids – disease association. This review also discusses the physiologic and genomic factors underlying these interethnic differences. Additionally, because of the importance of serum lipids in assessing disease risk, interethnic differences in serum lipids have implications for identifying African ancestry individuals at risk of cardiometabolic disease. Where possible, data from Africa is included, to further elucidate these ancestral differences in the context of a different environmental background.

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Section: The Metabolic Syndromementioning

confidence: 99%

“…In a Ugandan rural general population, 71.3% had low HDLC, but only 5% had high TG [73]. As seen among AA, higher abdominal obesity fuels higher MetSyn rates among women compared to men [36, 71]. …”

Section: The Metabolic Syndromementioning

confidence: 99%

Interethnic Differences in Serum Lipids and Implications for Cardiometabolic Disease Risk in African Ancestry Populations

Bentley¹,

Rotimi

2017

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“…Metabolic syndrome refers to a subset of metabolic abnormalities, which may increase the likelihood of developing cardiovascular disease and type II diabetes (1). In recent years, metabolic syndrome has become an increasing public health concern.…”

Section: Introductionmentioning

confidence: 99%

Epigallocatechin-3-gallate ameliorates insulin resistance in hepatocytes

Zhang

Miao

et al. 2017

Molecular Medicine Reports

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Hyperglycemia is a typical pathogenic factor in a series of complications among patients with type II diabetes. Epigallocatechin-3-gallate (EGCG) is the major polyphenol extracted from green tea and is reported to be an antioxidant. The aim of the present study was to examine the effect of EGCG on insulin resistance in human HepG2 cells pretreated with high concentrations of glucose. The protein kinase B (AKT)/glycogen synthase kinase (GSK) pathways were analyzed using western blot analysis in HepG2 cells and primary mouse hepatocytes treated with high glucose and/or EGCG. Cellular glycogen content was determined using a glycogen assay kit. Reactive oxygen species (ROS) production was determined using dihydroethidium staining and flow cytometry. c‑JUN N‑terminal kinase (JNK)/insulin receptor substrate 1 (IRS1)/AKT/GSK signaling was explored using western blot analysis in HepG2 cells treated with high glucose and/or EGCG or N-acetyl-cysteine. High glucose significantly decreased the levels of phosphorylated AKT and GSK in HepG2 cells and mouse primary hepatocytes. Pretreatment with EGCG significantly restored the activation of AKT and GSK in HepG2 cells and primary hepatocytes exposed to high glucose. In HepG2 cells and primary hepatocytes, glycogen synthesis was improved by EGCG treatment in a dose‑dependent manner. High glucose significantly stimulated the production of ROS while EGCG protected high glucose‑induced ROS production. ROS is known to serve a major role in high glucose induced‑insulin resistance by increasing JNK and IRS1 serine phosphorylation. In the present study, EGCG was observed to enhance the insulin‑signaling pathway. EGCG ameliorated high glucose‑induced insulin resistance in the hepatocytes by potentially decreasing ROS‑induced JNK/IRS1/AKT/GSK signaling.

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“…Homeostatic eating is need-based and replenishes energy storage, while hedonic eating is reward-driven and motivated by desire for palatable food [2]. As a causal factor, obesity is linked to increased risk of diseases such as diabetes [3, 4], cardiovascular disease (CVD) [5–7], cancer [8–10], arthritis [11, 12], infertility [13, 14], and mental health disorders [15, 16]. Importantly, new studies show that many of these pathways are regulated by epigenetic mechanisms that are disrupted by environmental factors.…”

Section: Introductionmentioning

confidence: 99%

An assessment of molecular pathways of obesity susceptible to nutrient, toxicant and genetically induced epigenetic perturbation

Xue

Ideraabdullah

2016

The Journal of Nutritional Biochemistry

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In recent years, the etiology of human disease has greatly improved with the inclusion of epigenetic mechanisms, in particular as a common link between environment and disease. However, for most diseases we lack a detailed interpretation of the epigenetic regulatory pathways perturbed by environment and causal mechanisms. Here, we focus on recent findings elucidating nutrient-related epigenetic changes linked to obesity. We highlight studies demonstrating that obesity is a complex disease linked to disruption of epigenetically regulated metabolic pathways in the brain, adipose tissue and liver. These pathways regulate (1) homeostatic and hedonic eating behaviors (2) adipocyte differentiation and fat accumulation, and (3) energy expenditure. By compiling these data we illustrate that obesity-related phenotypes are repeatedly linked to disruption of critical epigenetic mechanisms that regulate of key metabolic genes. These data are supported by genetic mutation of key epigenetic regulators and many of the diet induced epigenetic mechanisms of obesity are also perturbed by exposure to environmental toxicants. Identifying similarly perturbed epigenetic mechanisms in multiple experimental models of obesity strengthens the translational applications of these findings. We also discuss many of the ongoing challenges to understanding the role of environmentally-induced epigenetic pathways in obesity and suggest future studies to elucidate these roles. This assessment illustrates our current understanding of molecular pathways of obesity that are susceptible to environmental perturbation via epigenetic mechanisms. Thus, it lays the groundwork for dissecting the complex interactions between diet, genes, and toxicants that contribute to obesity and obesity-related phenotypes.

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High Prevalence of Abdominal Obesity Increases the Risk of the Metabolic Syndrome in Nigerian Type 2 Diabetes Patients: Using the International Diabetes Federation Worldwide Definition

Cited by 17 publications

References 42 publications

Interethnic Differences in Serum Lipids and Implications for Cardiometabolic Disease Risk in African Ancestry Populations

Interethnic Differences in Serum Lipids and Implications for Cardiometabolic Disease Risk in African Ancestry Populations

Epigallocatechin-3-gallate ameliorates insulin resistance in hepatocytes

An assessment of molecular pathways of obesity susceptible to nutrient, toxicant and genetically induced epigenetic perturbation

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