Adipose tissue malfunction leads to altered adipokine secretion which might consequently contribute to an array of metabolic diseases spectrum including obesity, diabetes mellitus, and cardiovascular disorders. Asprosin is a novel diabetogenic adipokine classified as a caudamin hormone protein. This adipokine is released from white adipose tissue during fasting and elicits glucogenic and orexigenic effects. Although white adipose tissue is the dominant source for this multitask adipokine, other tissues also may produce asprosin such as salivary glands, pancreatic B-cells, and cartilage. Significantly, plasma asprosin levels link to glucose metabolism, lipid profile, insulin resistance (IR), and β-cell function. Indeed, asprosin exhibits a potent role in the metabolic process, induces hepatic glucose production, and influences appetite behavior. Clinical and preclinical research showed dysregulated levels of circulating asprosin in several metabolic diseases including obesity, type 2 diabetes mellitus (T2DM), polycystic ovarian syndrome (PCOS), non-alcoholic fatty liver (NAFLD), and several types of cancer. This review provides a comprehensive overview of the asprosin role in the etiology and pathophysiological manifestations of these conditions. Asprosin could be a promising candidate for both novel pharmacological treatment strategies and diagnostic tools, although developing a better understanding of its function and signaling pathways is still needed.

White adipose tissue (WAT) is a specialized tissue whose main function is lipid synthesis and triglyceride storage. It is now considered as an active organ secreting a plethora of hormones and cytokines namely adipokines. Discovered in 1994, leptin has emerged as a key molecule with pleiotropic functions. It is primarily recognized for its role in regulating energy homeostasis and food intake. Currently, further evidence suggests its potent role in reproduction, glucose metabolism, hematopoiesis, and interaction with the immune system. It is implicated in both innate and adaptive immunity, and it is reported to contribute, with other adipokines, in the cross-talking networks involved in the pathogenesis of chronic inflammation and immune-related diseases of the musculo-skeletal system such as osteoarthritis (OA) and rheumatoid arthritis (RA). In this review, we summarize the most recent findings concerning the involvement of leptin in immunity and inflammatory responses in OA and RA.

Poly(3−hydroxybutyrate−co−3−hydroxyhexanoate) (PHBH) films were prepared using a cast film technique. Dioxane was chosen over other polymer solvents as it resulted in homogenous films with better morphology. Several plasticizers with different molecular weights and concentrations were added to the biopolymer solution prior to casting. Thermal, crystalline, and permeability properties were analyzed by thermogravimetric analysis (TGA), differential scanning calorimetry (DSC), X−ray diffraction (XRD), and both water vapor and oxygen transmission rate analysis. In general, the addition of plasticizers decreased the glass transition temperature (T_g), cold crystallization temperatures (T_cc), melting temperatures, as well as crystallinity degrees and increased the crystallite sizes and water vapor and oxygen transmission rates. The use of isosorbide and low-molecular-weight poly(ethylene glycol) (PEG) lowered the Tg around 30 °C at the highest used concentration, also being the most effective in increasing the crystallite size. When considering isosorbide and low-molecular-weight poly(ethylene glycol) (PEG) as very good plasticizers for PHBH, the question of which plasticizer to use strongly relies on the desired PHBH application.