Absence of in mouse pancreatic beta cells results in hyperinsulinemia.

Zinc is an essential component of the insulin protein complex synthesized in β cells. The intracellular compartmentalization and distribution of zinc are controlled by 24 transmembrane zinc transporters belonging to the ZnT or Zrt/Irt-like protein (ZIP) family. Downregulation of has been reported in pancreatic islets of patients with type 2 diabetes (T2D) as well as mouse models of high-fat diet (HFD)- or db/db-induced obesity.

Tailored Out-of-Oven Energy Efficient Manufacturing of High-Performance Composites with Two-Stage Self-Regulating Heating via a Double Positive Temperature Coefficient Effect.

The needs for sustainable development and energy efficient manufacturing are crucial in the development of future composite materials. Out-of-oven (OoO) curing of fiber-reinforced composites based on smart conductive polymers reduces energy consumption and self-regulates the heating temperature with enhanced safety in manufacturing, presenting an excellent example of such energy efficient approaches. However, achieving the desired curing processes, especially for high-performance systems where two-stage curing is often required, remains a great challenge.

Metal transporter SLC39A14/ZIP14 modulates regulation between the gut microbiome and host metabolism.

Metal transporter SLC39A14/ZIP14 is localized on the basolateral side of the intestine, functioning to transport metals from blood to intestine epithelial cells. Deletion of causes spontaneous intestinal permeability with low-grade chronic inflammation, mild hyperinsulinemia, and greater body fat with insulin resistance in adipose. Importantly, antibiotic treatment reverses the adipocyte phenotype of knockout (KO), suggesting a potential gut microbial role in the metabolic alterations in the KO mice.

Sucrose-induced hyperglycemia dysregulates intestinal zinc metabolism and integrity: risk factors for chronic diseases.

Objective: Zinc is an essential micronutrient that is critical for many physiological processes, including glucose metabolism, regulation of inflammation, and intestinal barrier function. Further, zinc dysregulation is associated with an increased risk of chronic inflammatory diseases such as type II diabetes, obesity, and inflammatory bowel disease. However, whether altered zinc status is a symptom or cause of disease onset remains unclear.

Intestine-specific deletion of metal transporter causes brain manganese overload and locomotor defects of manganism.

Impaired manganese (Mn) homeostasis can result in excess Mn accumulation in specific brain regions and neuropathology. Maintaining Mn homeostasis and detoxification is dependent on effective Mn elimination. Specific metal transporters control Mn homeostasis.