Programming of obesity and pediatric metabolic syndromes: a review in light of epigenetic modulation

Obesity is a multifactorial health problem characterized by the excessive accumulation of fat in the body and affects approximately 338 million children and adolescents worldwide. For this reason, this study consisted of a literature review to investigate how the causes and treatments of pediatric obesity are being addressed in light of epigenetic modulation as a factor in metabolic programming. For this, preferentially original articles published in English between the years 2017 to 2021 in the PubMed and Scholar Google databases were searched using the epigenetics descriptors; epigenetic modulation; child obesity; metabolic syndrome, combined with each other. A total of 54,000 articles were returned to searches in PubMed and 16,107,000 in Scholar Google. Fewer than 500 studies jointly addressed epigenetics and aspects of obesity or metabolic syndromes in childhood. Only 14 works matched the search criteria. The most discussed epigenetic mechanism in the literature is DNA methylation, whose rates observed mainly in CpG islands of promoter regions in several genes contribute to the prevention and early diagnosis of obesity and other pediatric comorbidities even before birth, based on the correlation between the epigenetic marks, maternal and paternal health and anthropometric indices. Although experimental studies on infant metabolic programming are scarce, existing knowledge suggests that environmental, nutritional, and energy expenditure changes are capable of modulating the epigenome and reversing marks that induce susceptibility to metabolic comorbidities.

A Comparative Study of Hypertension with and Without Metabolic Syndrome

Background: hypertension is prevalent in all the populations of world and is a serious risk factor for the patients . in many patients it is associated with metabolic syndrome which nearly doubles the risk . so we should investigate every patient with hypertension for with or without metabolic syndrome so as to save from its complications Methods: Sixty patients males and females coming in out patient door of Pak Red Crescent Medical College Dina Nath who on history physical examination and investigations were diagnosed as essential hypertension were investigated for further differentiation into with or without metabolic syndromes. Results: 21/60 patients with hypertension were found suffering from metabolic syndromes while 39/60 were not having metabolic syndrome. So a large number of patients were suffering from metabolic syndromes in our rural young population Conclusion: the prevalence of metabolic syndromes should be evaluated in all hypertension patients and all the factors of metabolic syndrome should be treated as well Keywords: Metabolic syndrome, essential hypertension, dyslipidemia

CYTOKINE RESISTIN IN METABOLIC AND CARDIOVASCULAR DISEASE.

The rise in metabolic syndromes is known to be the root cause of major cardiovascular diseases mainly Coronary Artery Disease (CAD) in India. A biological marker will thus help to determine the disease before its onset and help cure it at early stages, reducing the chances of development of further complications. There are various pro-inammatory markers (cytokines) which can be used to determine the onset of disease one such marker known is resistin. Resistin is known to be a pro-inammatory adipokine secreted mainly from Peripheral mononuclear cell (PMNC), bone marrow cells and macrophages in humans [1]. Inammatory response is generated due to rise in metabolic syndromes which in turn leads to the secretion of various cytokines. The levels of these cytokines released help in determining the severity of disease.

Obesity-linked circular RNA circTshz2-2 regulates the neuronal cell cycle and spatial memory in the brain

Metabolic syndromes, including obesity, cause neuropathophysiological changes in the brain, resulting in cognitive deficits. Only a few studies explored the contribution of non-coding genes in these pathophysiologies. Recently, we identified obesity-linked circular RNAs (circRNA) by analyzing the brain cortices of high-fat-fed obese mice. In this study, we scrutinized a conserved and neuron-specific circRNA, circTshz2-2, which affects neuronal cell cycle and spatial memory in the brain. Transcriptomic and cellular analysis indicated that circTshz2-2 dysregulation altered the expression of cell division-related genes and induced cell cycle arrest at the G2/M phase of the neuron. We found that circTshz2-2 bound to the YY1 transcriptional complex and suppressed Bdnf transcription. Suppression of circTshz2-2 increased BDNF expression and reduced G2/M checkpoint proteins such as Cyclin B2 and CDK1 through BDNF/TrkB signaling pathway, resulting in cell cycle arrest and neurite elongation. Inversely, overexpression of circTshz2-2 decreased BDNF expression, induced cell cycle proteins, and shortened the neurite length, indicating that circTshz2-2 regulates neuronal cell cycle and structure. Finally, we showed that circTshz2-2 affects spatial memory in wild-type and obese mice. Our data have revealed potential regulatory roles of obesity-related circTshz2-2 on the neuronal cell cycle and memory function providing a novel link between metabolic syndromes and cognitive deficits.

The Role of Bioactive Peptides in Diabetes and Obesity

Bioactive peptides are present in most soy products and eggs and have essential protective functions. Infection is a core feature of innate immunity that affects blood pressure and the glucose level, and ageing can be delayed by killing senescent cells. Food also encrypts bioactive peptides and protein sequences produced through proteolysis or food processing. Unique food protein fragments can improve human health and avoid metabolic diseases, inflammation, hypertension, obesity, and diabetes mellitus. This review focuses on drug targets and fundamental mechanisms of bioactive peptides on metabolic syndromes, namely obesity and type 2 diabetes, to provide new ideas and knowledge on the ability of bioactive peptide to control metabolic syndromes.