Study finds small colony of neurons modulate amount of insulin the pancreas produces.
The brain is the key regulator of appetite, body weight, and metabolism, controlling the passage of every nutrient that enters and exits the body. Specifically, there is a small group of hypothalamus neurons, named the Proopiomelanocortin neurons (POMC) capable of detecting and integrating signals to activate the appropriate physiological responses. These neurons are sensitive to fluctuations in nutrients such as glucose, fatty acids, and amino acids, however, the sensing mechanisms in POMC neurons are poorly understood. Now, a study led by researchers at IRB Barcelona describes the connection between POMC neurons in the hypothalamus and the release of insulin by the pancreas to identify new molecular mechanisms involved in this pathway. The team states their study shows Mitofusin-1, a protein-based mediator of mitochondrial fusion, pairs POMC neuron’s nutrient-sensing facility with systemic glucose metabolism. The study is published in the journal Cell Metabolism.
Previous studies show POMC neurons can detect changes in nutrient availability, with the molecular basis involved in their ability to detect fluctuations in nutrients linked to changes in the shape of mitochondria. The phenomenon of mitochondrial deformation is known as mitochondrial dynamics, a mechanism of energy adaptation in changing metabolic conditions to adjust the needs of cells. The current study investigates whether defects in the mitochondrial dynamics of POMC neurons can cause alterations in metabolism.
The current study ablates the mitochondrial dynamics protein, Mitofusin-1, in the POMC cells of mice. Results show mice bred without this mitochondrial dynamics protein have altered glucose levels. Data findings show defects in mitochondrial dynamics lead to disturbances in glucose metabolism which are caused by a lower secretion of insulin.
Results show POMC neurons are involved in the control of the intake and the amount of insulin secreted by the beta cells of the pancreas. Data findings show this communication between the hypothalamus and the pancreas depends on the activity of the protein Mitofusin-1. The group explains the alterations are due to a disproportionate, though transitory, increase in the production of radical oxygen species in the hypothalamus. They go on to add when the levels of radical oxygen species in the hypothalamus are restored in the laboratory, the pancreas starts to secrete the correct levels of insulin again.
The team surmises their data shows mitochondrial dynamics in POMC neurons mediated by Mitofusin-1 are an intrinsic nutrient-sensing mechanism. For the future, the researchers state understanding the mechanisms involved in regulating insulin is important and helps to better understand the pathology of diabetes.
Source: Institute for Research in Biomedicine (IRB Barcelona)
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Michelle Petersen View All
I am an award-winning science journalist and health industry veteran who has taught and worked in the field.
Featured by numerous prestigious brands and publishers, I specialize in clinical trial innovation–-expertise I gained while working in multiple positions within the private sector, the NHS, and Oxford University, where I taught undergraduates the spectrum of biological sciences integrating physics for over four years.
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