Effect of High Glucose Levels on White Adipose Cells and Adipokines—Fuel for the Fire

Abstract

White adipocytes release adipokines that influence metabolic and vascular health. Hypertrophic obesity is associated with adipose tissue malfunctioning, leading to inflammation and insulin resistance. When pancreatic islet β cells can no longer compensate, the blood glucose concentration rises (hyperglycemia), resulting in type 2 diabetes. Hyperglycaemia may further aggravate adipose cell dysfunction in ~90% of patients with type 2 diabetes who are obese or overweight. This review will focus on the effects of high glucose levels on human adipose cells and the regulation of adipokines.

Hyperglycemia Affects miRNAs Expression Pattern during Adipogenesis of Human Visceral Adipocytes—Is Memorization Involved?

“…Bioinformatics analysis also underscored the well-known endocrine function of Ads, showing records with IL-6, leptin, adiponectin, etc. [ 5 ]. To better understand the role of each of the 15 selected miRNAs, we presented the top three records for each molecule (DIANA-miRPath) ( Material S1, (Table S7) ).…”

“…The expansion of visceral fat (measured as the waist-to-hip ratio, WHR) is a strong predictor for T2DM development, which is inseparably connected with raised blood glucose levels [ 4 ]. Hyperglycemia (HG) exerts an impact on each body cell while occurring chronically and acutely, including mature adipocytes treated with high and normal glucose interchangeably for 24 h [ 5 , 6 ]. HG is infamous for being especially detrimental to endothelial cells, where it promotes metabolic memory via epigenetic mechanisms that are mediated, among others, by microRNAs (miRNAs) [ 7 , 8 , 9 ].…”

Influence of Nutritional Intake of Carbohydrates on Mitochondrial Structure, Dynamics, and Functions during Adipogenesis

“…Differentiation induction is related to a significant increase at the transcriptional level of the adipogenesis master regulator, peroxisome proliferator-activated receptor γ (PPARγ), during the early adipogenesis phase yet significantly lower in the LG-GAL condition ( Figure 2 (A1)). In parallel, the expression of PREF-1, an autocrine and paracrine factor preventing the advancement to mature adipocytes [ 38 , 39 , 40 ], has been evaluated at the transcriptional level in both conditions. The results show a significant decrease of this adipogenesis repressor in both conditions, although to a lesser extent in the LG-GAL condition ( Figure 2 (A2)).…”

“…In both physiological and pathological contexts, adipogenesis is known to be highly sensitive to the nutritional composition. Especially, changes in the carbohydrates resources are expected to modulate this differentiation process [ 40 , 42 , 51 , 52 , 53 ]. As obesity and co-morbidities are increasing worldwide, (re)considering the nutritional qualitative and quantitative parameters as a strategy to improve the management of those diseases seems to be decisive.…”

“…In addition, various compositions of carbohydrate diet were evaluated to reduce insulin resistance and other systemic metabolic homeostasis consequences linked to supraphysiological glucose levels and their associated glucotoxic effects in several organs [ 35 , 36 , 37 , 38 ]. Among them, the WAT, which is known as a huge glucose consumer and storage tissue, is sensitive to environmental carbohydrates levels to promote remodeling mechanisms observed in an obesity context [ 39 , 40 , 41 ]. In an interesting way, 3T3-L1 adipogenesis was demonstrated to be influenced by the carbohydrate’s quality parameter, indicating how crucial this nutritional factor can be [ 42 ].…”