Background: Connexin proteins are essential for cell differentiation, function, and survival. Results: Global deletion of Cx37 results in increased bone mass caused by reduced osteoclast maturation. Conclusion: Our findings demonstrate a previously unrecognized role of Cx37 in bone homeostasis in vivo. Significance: Therapeutic approaches to increase bone mass might be developed by interfering with Cx37 function.

Connexin43 (Cx43) forms gap junction channels and hemichannels that allow the communication among osteocytes, osteoblasts, and osteoclasts. Cx43 carboxy-terminal (CT) domain regulates channel opening and intracellular signaling by acting as a scaffold for structural and signaling proteins. To determine the role of Cx43 CT domain in bone, mice in which one allele of full length Cx43 was replaced by a mutant lacking the CT domain (Cx43ΔCT/fl) were studied. Cx43ΔCT/fl mice exhibit lower cancellous bone volume but higher cortical thickness than Cx43fl/fl controls, indicating that the CT domain is involved in normal cancellous bone gain but opposes cortical bone acquisition. Further, Cx43ΔCT is able to exert the functions of full length osteocytic Cx43 on cortical bone geometry and mechanical properties, demonstrating that domains other than the CT are responsible for Cx43 function in cortical bone. In addition, parathyroid hormone (PTH) failed to increase endocortical bone formation or energy to failure, a mechanical property that indicates resistance to fracture, in cortical bone in Cx43ΔCT mice with or without osteocytic full length Cx43. On the other hand, bone mass and bone formation markers were increased by the hormone in all mouse models, regardless of whether full length or Cx43ΔCT were or not expressed. We conclude that Cx43 CT domain is involved in proper bone acquisition; and that Cx43 expression in osteocytes is dispensable for some but not all PTH anabolic actions.

Our findings demonstrate that Kir4.1 channels possess a diurnal rhythm, and this rhythm is dampened with diabetes, thereby suggesting that the increase in TNF-α is detrimental to normal Kir4.1 rhythm and expression.

Background: Diabetes mellitus is a global health problem leading to an increase in the search for herbal normoglycaemic agents as alternative to the synthetic ones. Aqueous extract of Parkia biglobosa leaves was assessed for normoglycaemic effects in alloxan-induced diabetic rats. The study aim at providing scientific evidence to authenticate the traditional use of Parkia biglobosa leaves in the treatment of diabetes. Methodology: The plant was extracted using aqueous to obtain Parkia biglobosa Leaf Extract (PbLE), qualitative phytochemical analysis was determined using standard methods. Diabetes was induced in albino rats by intraperitoneal injection of 5% solution of alloxan (150 mg/kg bw). The rats were grouped into 5 groups (A, B, C, D and E) of 5 animals each. Group A consisted of non-diabetic rats which served as the control, Group B consisted of diabetic rats that were left untreated and served as negative control, Group C were given glucophage (reference) at a dose level of 7 mg/kg bw, Groups D and E were administered PbLE at the doses of 250 and 500 mg/kg bw respectively. Results: The glucose levels in the blood of rats were checked with a glucometer using the blood from the tail of the rats. Serum (proteins, lipid profiles, urea and creatinine), ALT, AST and ALP were all determined using standard procedures. The extract and the glucophage reduced the blood glucose level significantly (p < 0.05) from day 3 till the termination of the experiment.                                                                                                                                                Conclusion: Aqueous extract of Parkia biglobosa leaves possess antidiabetic activity and also the extract is relatively safe.  Hence the leaves of Parkia biglobosa can be explored in producing alternative antidiabetic drugs.