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Researchers examine adipocyte communication in metabolic processes


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3 minutes

Jonathan Z. Long, PhD
Jonathan Z. Long, PhD

New and emerging research continues to shed light on the role of adipocytes in the function and regulation of diverse metabolic processes. During this year’s ADA Diabetes Journal Symposium: Staying in Network—Adipocyte Communication in Regulation of Energy Balance, investigators will share findings from studies exploring adipocyte response to physiologic and metabolic cues.

The session will be held on Sunday, June 25, at 8:00 a.m. PT in Ballroom 6C-F of the San Diego Convention Center.

Jonathan Z. Long, PhD, Assistant Professor of Pathology at Stanford University, will describe research looking at signaling pathways in energy metabolism, including exercise-induced mediators of body adiposity.

“There is a significant interest in identifying blood-borne factors that mediate tissue crosstalk and function as molecular effectors of physical activity,” Dr. Long said. “Although past studies have focused on an individual molecule or cell type, the organism-wide secretome response to physical activity has not been evaluated.”

He and his colleagues used a cell-type-specific proteomic approach to generate a 21-cell-type, 10-tissue map of exercise training-regulated secretomes in mice. Their current dataset identifies more than 200 exercise training-regulated cell-type-secreted protein pairs, the majority of which have not been previously reported, he said.

Renata Pereira, PhD
Renata Pereira, PhD

Among their findings, they showed that Pdgfra-cre-labeled secretomes were the most responsive to exercise training. Dr. Long said the further identification of specific molecular effectors of physical activity may enable therapeutic and pharmacological “capture” of the cardiometabolic benefits of exercise.

Renata Pereira, PhD, Assistant Professor of Internal Medicine at the University of Iowa Fraternal Order of Eagles Diabetes Research Center, will discuss mitochondrial dynamics in adipose tissue biology and in the pathophysiology of diet-induced insulin resistance.

She will review findings from a study that compared data collected from mice lacking the mitochondrial fusion protein optic atrophy 1 (OPA1) specifically in brown adipocytes versus mice lacking OPA1 in both brown and white adipocytes.

“Our data showed that OPA1 deletion in brown adipocytes led to compensatory mechanisms that improved metabolic health and promoted resistance to diet-induced obesity and insulin resistance,” Dr. Pereira said.

Conversely, she noted that OPA1 deletion in both brown and white adipocytes resulted in lipodystrophy and impaired glucose homeostasis, primarily due to compromised lipid metabolism, increased inflammation, and white adipocyte senescence.

James C. Lo, MD, PhD
James C. Lo, MD, PhD

“OPA1 is crucial to regulate lipid storage and mobilization in white adipocytes, and its expression in white adipocytes is required for the compensatory mechanisms observed when OPA1 is downregulated exclusively in brown adipocytes, including browning of white adipocytes,” Dr. Pereira said. “These data indicate that inducing OPA1 expression in white adipocytes might improve adipose tissue function in the context of obesity, thereby attenuating diet-induced insulin resistance.”

James C. Lo, MD, PhD, Associate Professor of Medicine at Weill Cornell Medical College, will discuss research exploring inputs from outside and within the pancreas that might affect beta cell function and fate.

“We found that adipsin, a factor made by fat cells, can protect the insulin-producing beta cells. Our work also identifies different subsets of beta cells that may be critically lost and contribute to the development of diabetes,” Dr. Lo said. “Our findings inform on why beta cells could malfunction in type 2 diabetes. This could inform future therapies that limit beta cell loss that could prevent type 2 diabetes and/or its complications.”

Li Ye, PhD, Associate Professor in the Department of Neuroscience at Scripps Research, will discuss the role of somatosensory innervation of adipose tissues.