Effects and mechanisms of nutritional interventions on extradigestive complications in obese patients.

BACKGROUND: Obesity is associated with an increased risk of multiple extradigestive complications. Thus, understanding the global epidemiology of obesity and its relationship with extradigestive complications, such as cardiovascular disease, type 2 diabetes mellitus, and non-alcoholic fatty liver disease is important. However, nutritional intervention can positively manage issues associated with obesity. Hence, the identification of the current high prevalence of extradigestive complications among patients with obesity and the potential role of nutritional interventions is also essential. AIM: To determine the relationship between obesity and extradigestive complications and emphasize the importance of nutritional interventions in the management of patients with obesity. METHODS: Overall, 110 patients with obesity admitted to our hospital from February 2020 to November 2022 and 100 healthy individuals were included in the present study. Information of the study population, including demographic characteristics, such as age, sex, body mass index, indicators of extradigestive complications, dietary intake, and biomarkers was collected. The study design, participant selection, interventions, and development of the nutritional intervention program were described. The collected data were analyzed to assess the effect of nutritional interventions on extradigestive complications. RESULTS: As a part of nutritional intervention, the dietary structure was modified to decrease the saturated fatty acid and cholesterol intake and increase the dietary fiber and polyunsaturated fatty acid intake to improve the blood lipid levels and cardiovascular health. Mechanistic studies showed that these nutritional interventions positively affected mechanisms that regulate lipid metabolism, improved inflammatory markers in the blood, and improved vascular functions. CONCLUSION: The study discusses the consistency of the present results with previous findings to assess the clinical significance of the present findings. The study provides direction for future research on improving nutritional intervention strategies.

TNF-α, IL-6, and leptin increase the expression of miR-378, an adipogenesis-related microRNA in human adipocytes.

Obesity has become a global public health problem associated with complications including type 2 diabetes, cardiovascular disease, and several cancers. Adipocyte differentiation (adipogenesis) plays an important role in obesity and energy homeostasis. Adipose tissue secretes multiple cytokines and adipokines which can cause the complications of obesity, especially insulin resistance. TNF-α, IL-6, leptin, and resistin have been identified as the main regulators of obesity and insulin activity. miR-378 is highly induced during adipogenesis and has been reported to be positively regulated in adipogenesis. In the current study, matured human adipocytes were treated with TNF-α, IL-6, leptin, or resistin on the 15th day after the induction of human pre-adipocyte differentiation. We demonstrated that TNF-α, IL-6, and leptin upregulated miR-378 expression indicating that miR-378 probably is a novel mediator in the development of insulin resistance related to obesity.

MiR-335, an adipogenesis-related microRNA, is involved in adipose tissue inflammation.

During the development of obesity, adipose tissue releases a host of different adipokines and inflammatory cytokines, such as leptin, resistin, tumor necrosis factor α (TNF-α), Interleukin-6 (IL-6), and adiponectin, which mediate insulin resistance. Recently, some microRNAs (miRNAs) regulated by adiponectin were identified as novel targets for controlling adipose tissue inflammation. Therefore, the relationship between adipokines and miRNA is worth studying. MiR-335 is an adipogenesis-related miRNA and implicated in both fatty acid metabolism and lipogenesis. In this study, we focused on the association of miR-335 and adipokines, and examined the expression trend of miR-335 during human adipocyte differentiation. Our results showed that miR-335 is significantly upregulated with treatment of leptin, resistin, TNF-α, and IL-6 in human mature adipocytes, and its expression elevated in the process of adipocyte differentiation. Interestingly, the transcriptional regulation of miR-335 by these adipokines seems independent of its host gene (mesoderm-specific transcript homolog, MEST). Thus, we cloned and identified potential promoter of miR-335 within the intron of MEST. As a result, a fragment about 600-bp length upstream sequences of miR-335 had apparent transcription activity. These findings indicated a novel role for miR-335 in adipose tissue inflammation, and miR-335 might play an important role in the process of obesity complications via its own transcription mechanism.