Monomeric cocoa catechins enhance β-cell function by increasing mitochondrial respiration.

A hallmark of type 2 diabetes (T2D) is β-cell dysfunction and the eventual loss of functional β-cell mass. Therefore, mechanisms that improve or preserve β-cell function could be used to improve the quality of life of individuals with T2D. Studies have shown that monomeric, oligomeric and polymeric cocoa flavanols have different effects on obesity, insulin resistance and glucose tolerance.

Mechanisms by which cocoa flavanols improve metabolic syndrome and related disorders.

Dietary administration of cocoa flavanols may be an effective complementary strategy for alleviation or prevention of metabolic syndrome, particularly glucose intolerance. The complex flavanol composition of cocoa provides the ability to interact with a variety of molecules, thus allowing numerous opportunities to ameliorate metabolic diseases. These interactions likely occur primarily in the gastrointestinal tract, where native cocoa flavanol concentration is high.

HCN1 channels as targets for anesthetic and nonanesthetic propofol analogs in the amelioration of mechanical and thermal hyperalgesia in a mouse model of neuropathic pain.

Chronic pain after peripheral nerve injury is associated with afferent hyperexcitability and upregulation of hyperpolarization-activated, cyclic nucleotide-regulated (HCN)-mediated IH pacemaker currents in sensory neurons. HCN channels thus constitute an attractive target for treating chronic pain. HCN channels are ubiquitously expressed; analgesics targeting HCN1-rich cells in the peripheral nervous system must spare the cardiac pacemaker current (carried mostly by HCN2 and HCN4) and the central nervous system (where all four isoforms are expressed).

Role of capsaicin in a murine model of labor and delivery.

Background: The objectives of this study were to develop a murine model of labor and delivery and to use this model to examine whether capsaicin diminishes labor pain and expedites delivery.

Methods: To develop a murine model of labor pain, the authors identified and compared the incidence of four proposed pain behaviors in 46 mice: (1) No analgesia in labor and the postpartum period, and (2) increasing doses of an analgesic, morphine. The model was then used to examine the impact of topical cervical capsaicin on: (1) labor pain behaviors and (2) labor progress by examining its impact on the time from treatment to delivery of the first pup and on the duration of delivery per pup.

The antinociceptive response to nicotinic agonists in a mouse model of postoperative pain.

Background: Nicotine, the prototypical broad spectrum agonist at central nicotinic receptors, has analgesic action after surgery. Various subtype-specific nicotinic agonists have antinociceptive effects in animal models, but the response is highly dependent on the model tested. In an effort to determine what nicotinic subtypes might be targeted in future clinical studies, we tested agonists selective for alpha 4 beta 2 and alpha 7 containing nicotinic receptors in a mouse model of postoperative pain.

Isoflurane prevents nicotine-evoked norepinephrine release from the mouse spinal cord at low clinical concentrations.

Background: Volatile anesthetics inhibit nicotinic acetylcholine receptors at subanesthetic concentrations. In both animal and human studies, similar concentrations of volatile anesthetics have been associated with increased sensitivity to pain. Nicotinic analgesia is thought to involve the enhanced release of norepinephrine.

The role of adrenergic and cholinergic transmission in volatile anesthetic-induced pain enhancement.

Volatile anesthetic drugs have a biphasic effect on pain transmission. At very small concentrations they enhance pain sensitivity whereas at larger subanesthetic concentrations they have an analgesic effect. Previous work has suggested that nicotinic inhibition could mediate the pronociceptive action of isoflurane.