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Molecular Pharmacology article by Drs. Haj and Bettaieb selected for research highlights by journal

haj-bettaieb-article2Multiple Haj lab members are co-authors on a recently published article in Molecular Pharmacology that was selected for research highlights by the journal.   The article was selected as one of the journal highlights that was posted this month on the ASPET website. The paper was also announced on Twitter (Mol Pharm (ASPET) @MolPharmJournal) and announced on Molecular Pharmacology’s Facebook page.

The article abstract is available online.

 

Refrerence

Bettaieb A1, Chahed S1, Bachaalany S1, Griffey S1, Hammock BD1, Haj FG2. Soluble Epoxide Hydrolase Pharmacological Inhibition Ameliorates Experimental Acute Pancreatitis in Mice.. Mol Pharmacol. 2015 Aug;88(2):281-90. [PubMed]

 

Drs. Haj and Bettaieb among group of scientists who find key mechanism that causes neuropathic pain

haj-bettaieb-articleScientists at the University of California, Davis, have identified a key mechanism in neuropathic pain. The discovery could eventually benefit millions of patients with chronic pain from trauma, diabetes, shingles, multiple sclerosis or other conditions that cause nerve damage.

A biological process called endoplasmic reticulum stress, or ER stress, is the significant driver of neuropathic pain, said lead researchers Bora Inceoglu of the UC Davis Department of Entomology and Nematology and UC Davis Comprehensive Cancer Center, and Ahmed Bettaieb, Department of Nutrition. The work is published July 6 in the journal Proceedings of the National Academy of Sciences.

“This is a fundamental discovery that opens new ways to control chronic pain,” said co-author Bruce Hammock, distinguished professor at the UC Davis Department of Entomology and Nematology and the UC Davis Comprehensive Cancer Center.

“We can now specifically search for agents to control ER stress and its downstream pathways,” Hammock said. “This search is already underway in a number of laboratories working on cancer and other diseases.”

Working with Professor Fawaz Haj of the UC Davis nutrition department, Bettaieb found that key molecular signatures associated with diabetes and diabetic pain were linked to ER stress. Neuropathic pain is a common consequence of both Type 1 and Type 2 diabetes, affecting up to 70 percent of patients.

Inceoglu, working in Hammock’s laboratory, showed that neuropathic pain could be initiated by compounds that cause ER stress and reversed by agents that block it.

The researchers had previously shown that a class of natural bioactive lipids has powerful analgesic effects in the body. These analgesic lipids are broken down in the body by an enzyme, soluble epoxide hydrolase. The team was able to show that blocking soluble epoxide hydrolase blocks ER stress and associated neuropathic pain.

The work sheds new light onto at least one biological process that mediates neuropathic pain, Inceoglu said. With this knowledge, researchers can now test ER-stress blocking drugs in the clinic, and carry out fundamental research on how different types of pain grouped under the name “neuropathic” differ from each other and respond to new drugs.

The study provides convincing evidence for a novel concept as to what causes neuropathic pain said John Imig, professor of pharmacology and toxicology at the Medical College of Wisconsin, Milwaukee, who was not involved in the study. The work provides new opportunities for drugs or drug combinations to treat chronic pain, he said.

Additional authors on the paper are Kin Sing Stephen Lee and Carlos Trindade da Silva, both at the UC Davis Department of Entomology and Nematology and the UC Davis Comprehensive Cancer Center.

The research was supported by grants from the National Institute of Environmental Health Sciences and NIEHS Superfund Basic Research Program grant, National Institutes of Health, and the National Institute of Arthritis and Musculoskeletal and Skin Disease.

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From UC Davis News

Dr. Fawaz Haj to collaborate on new NIH grant to fund mouse-based research center at UC Davis

Dr. Haj will be a collaborator on a new National Institutes of Health grant that awarded $3.8 million to the University of California, Davis, to fund a new mouse-based research center devoted to studies of the physiology and genetics of obesity, diabetes and cardiovascular health.

A major focus for the new Mouse Metabolic Phenotyping Center will be cardiovascular disease, which affects more than 82 million Americans, costs an estimated $444 billion annually and is the nation’s leading cause of death.

The new center will provide scientists worldwide with complete physiologic characterizations of mice that have been genetically altered for metabolic studies. It will be one of only six such centers in the United States, and the only one that can create the mice for researchers.

Collaborating in the new center are UC Davis School of Medicine researchers Craig Warden, scientific director of the Mouse Metabolic Phenotyping Center and a professor of pediatrics, and neurobiology, physiology and behavior; Amparo Villablanca and Nipavan Chiamvimovat, both professors of cardiovascular medicine; Liming Jin, an assistant professor of endocrinology; and Thomas Huser, an adjunct professor of endocrinology.

Collaborators from the School of Veterinary Medicine include clinical professor Stephen Griffey; Peter Havel, a professor of molecular bioscience; Philip Kass, a professor of statistics; Jon Ramsey, an associate professor of molecular bioscience; Helen Raybould, a professor of physiology; and assistant clinical professor Katherine Wasson.

Other collaborators include adjunct assistant nutrition professor Sean H. Adams, a supervisory research physiologist at the USDA-Agricultural Research Service’s Western Human Nutrition Research Center at UC Davis; and Mari Golub, an adjunct professor of toxicology.

Dr. Fawaz Haj is co-author on article suggesting leptin may offer Type 2 diabetes treatment

The hormone leptin, naturally produced by fat cells and long known to play an important role in regulating appetite and fat metabolism, may prove to be successful in treating Type 2 diabetes, a disease that affects more than 21 million people in the United States, reports a team of scientists led by researchers at the University of California, Davis.

The findings from their study, involving rats predisposed to Type 2 diabetes — formerly known as adult-onset diabetes — appear in the Aug. 30 issue of the journal the Proceedings of the National Academy of Sciences.

“One of leptin’s important effects is in signaling the brain to decrease food intake, and recent animal studies have shown that the hormone also lowers blood sugar in Type 1 diabetes,” said lead author Peter Havel, a veterinary endocrinologist.

“Our study, however, is the first to demonstrate that twice-daily injections of leptin lower blood sugar levels and circulating triglycerides in an animal model with the more common form of diabetes — Type 2 diabetes,” Havel said.

Triglycerides are compounds containing three fatty acids; they primarily circulate in the bloodstream and, at high levels, can increase the risk of heart disease.

“The data from this study indicate that leptin improves blood sugar control, in part, by increasing the animals’ sensitivity to insulin, the hormone responsible for maintaining normal blood sugar levels,” said co-author Bethany Cummings, a veterinary molecular physiologist in the Havel laboratory.

The results suggest that the improved insulin sensitivity may be due to reduced stress in a specialized part of the cell called the endoplasmic reticulum. Previous studies have shown that stress to the endoplasmic reticulum can cause insulin resistance, which can lead to Type 2 diabetes.

The study also showed that the leptin treatments resulted in decreased levels of circulating glucagon, a hormone produced in the pancreas that stimulates an increase in blood-sugar levels and works in opposition to insulin.

Other co-authors of this study are: postdoctoral fellow Ahmed Bettaieb, Associate Professor Fawaz G. Haj, and undergraduate assistant Riva Dill, all of the UC Davis Department of Nutrition; research scientists James L. Graham and Kimber L. Stanhope, both of the School of Veterinary Medicine and the Department of Nutrition; and Research Assistant Professor Gregory J. Morton of the University of Washington School of Medicine.

Funding for the study was provided by the National Institutes of Health and UC Davis’ Center for Nutrition and Health Research.

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