Quenching and quorum sensing in bacterial bio-films.

Quorum sensing (QS) is the ability of bacteria to monitor their population density and adjust gene expression accordingly. QS-regulated processes include host-microbe interactions, horizontal gene transfer, and multicellular behaviours (such as the growth and development of biofilm). The creation, transfer, and perception of bacterial chemicals known as autoinducers or QS signals are necessary for QS signalling (e.g. N-acylhomoserine lactones). Quorum quenching (QQ), another name for the disruption of QS signalling, comprises a wide range of events and mechanisms that are described and analysed in this study. In order to better comprehend the targets of the QQ phenomena that organisms have naturally developed and are currently being actively researched from practical perspectives, we first surveyed the diversity of QS-signals and QS-associated responses. Next, the mechanisms, molecular players, and targets related to QS interference are discussed, with a focus on natural QQ enzymes and compounds that function as QS inhibitors. To illustrate the processes and biological functions of QS inhibition in microbe-microbe and host-microbe interactions, a few QQ paradigms are described in detail. Finally, certain QQ techniques are offered as potential instruments in a variety of industries, including agriculture, medical, aquaculture, crop production, and anti-biofouling areas.

Fibroblast growth factor 21 as a potential master regulator in metabolic disorders.

FGF21 is an endocrine hormone that controls key metabolic processes and induces the synthesis of glucose transporters, resulting in increased glucose absorption levels in fat cells. It is expressed in multiple metabolically active organs and tissues. FGF21 is also a powerful regulator of glucose homeostasis as a direct downregulating gene of peroxisome proliferator-activated receptor (PPAR), which plays a role in regulating the activity of glucose and lipids. Attempts were made to understand various aspects related to FGF21, including properties like receptor binding and genomic linkage map, along with the information about the genes that function in the upregulation of FGF21 and how it, directly and indirectly, downregulates the genes that are vital in various metabolic pathways. Furthermore, various gene regulatory analyses on the specific gene concerning unique micro RNAs and long non-coding RNAs that target FGF21 and alter its functioning along with single-nucleotide polymorphisms (SNPs) were observed, that are the common cause of cell dysregulation, leading to different metabolic diseases and pathogenesis of cancer. Unique protein-protein interaction and cross talk between FGF21 and PPARγ shed light on their combined role in metabolic disorder-related regulatory activities. Its potential and unique role as an effective biomarker for various cardiovascular and metabolic disorders have also been highlighted. This study attempts to highlight the pleiotropic role of FGF21 activity following its overexpression and inhibition of cascades that results in the induction of obesity from diet and simultaneously signals adipocytes to absorb glucose and decrease triglyceride and blood sugar levels in diabetic models (after administration), rendering it a promising treatment for several metabolic and cardiovascular disorders.

Effect of different dietary fats on inflammation and glucose intolerance in high fructose and high fat fed experimental animals.

OBJECTIVES: Diet is the major modifiable risk factor for the onset of insulin resistance and its progression into diabetes. In the present study the effect of various dietary fats on inflammatory homeostasis and glucose tolerance is investigated in high fat and high fructose fed mice model. METHODS: C57/BL6J mice were divided into four groups and fed a casein-based diet containing high fructose (45%) and high fat (24%) (clarified butter oil [CBO]; safflower oil [SFFO] and lard oil [LO]) for 120 days; oral glucose tolerance (OGTT), plasma lipid profile and plasma & adipose tissue cytokines levels were compared with the control diet (10% groundnut oil and 59.5% starch) fed animals. RESULTS: The total cholesterol and triglycerides were higher in CBO and LO fed animals with glucose intolerance and increased body weights; liver and white adipose tissue weights were higher in CBO and LO fed animals respectively. CBO feeding increased the plasma (IFN-γ) and adipose tissue cytokines (IFN-γ, IL-10, IL-6 & TNF-α). LO feeding increased plasma IFN-γ, TNF-α and IL-1ß and adipose tissue IL-6. SFFO feeding decreased body weight and tissue cytokines and increased plasma IFN-γ levels without causing impairment in the glucose tolerance. CONCLUSIONS: Consumption of a high fructose and high fat diet which mimic the present-day dietary pattern resulted in altered inflammatory homeostasis and impairment in glucose tolerance in 24% CBO and LO fed animals. The deleterious effects of high fructose feeding were reversed in SFFO fed mice possibly due to the presence of oleic and linoleic acids.

Attenuation of FGF21 signalling might aggravate the impairment of glucose homeostasis during the high sucrose diet induced transition from prediabetes to diabetes in WNIN/GR-Ob rats.

Fibroblast growth factor 21 (FGF21) has emerged as a pleiotropic hormone and is known for its beneficiary roles in the management of diabetes and hyperglycaemia. However, the role of FGF21 during the transition from prediabetes to diabetes still remains unclear. Hence, the present study is aimed to understand the regulation of glucose homeostasis by FGF21 during the transition from prediabetes to diabetes in WNIN/GR-Ob rats. A total of 36 WNIN/GR-Ob obese male rats (28 days old) were divided into control and high sucrose (HS) groups and were fed ad libitum with their respective diets. These groups were sacrificed at different time points (week 1, 6, and 12) and various physical, biochemical, and molecular mediators were assessed to address FGF21 mediated glucose homeostasis. The study results revealed that rats developed impaired glucose tolerance and insulin resistance by exhibiting delayed glucose clearance from circulation, elevated fasting insulin, increased AUC glucose and HOMA-IR scores significantly; thereby rats demonstrated prediabetes by week 6 and diabetes complications by week 12. In line with the above, differential expression of genes attributed to FGF21 mediated glucose homeostasis, i.e., PPARα, FGF21, ß-klotho, PPARγ, Adiponectin, Akt, and UCP1 suggest that the acute insulin sensitizing effect of FGF21 was significantly impaired during prediabetes to diabetes transition. In addition, increased gene and protein expression of FGF21 during the transition compared to controls could be a compensatory response to possibly counteract the metabolic stress imposed by high sucrose diet in WNIN/GR-Ob rats of the experimental group. Findings from the current study emphasize the potential role of FGF21 in glucose homeostasis and its attenuation might aggravate glucose impairment during the transition from prediabetes to diabetes in high sucrose diet induced WNIN/GR-Ob rats.

Strain specific variation underlines the disparity in stress response of rats to calorie dense diets in the pathophysiology of obesity.

Obesity is a multifactorial disorder, caused mainly due to lifestyle changes, and increased consumption of calorie dense diets is not just limited to developed countries anymore. Chronic physiological stress and oxidative stress are known to be implicated in the etiology of obesity. However, the role of stress response towards obesity manifestation in genetically different rat strains is poorly understood. In the current study we have used obesity susceptible & resistant rat models to understand the role of both glucocorticoid and oxidativestress in the pathophysiology of obesity. Upon challenge with calorie dense diets, WNIN showed an increased glucocorticoid stress, resulting in increased oxidative stress; whereas such a phenomenon was not noticed in F-344 and SD. However, there was an increase in the circulatory melatonin levels in calorie dense fed groups of both F-344 and SD animals, which might have contributed to reduced oxidative stress. The molecular switch in the activation of melatonin could be possibly attributed to the genetic differences among these strains. It will be interesting to explore other molecular mechanisms for melatonin regulation, albeit increased corticosterone is implicated in the enhanced production of melatonin.