A TRP channel contributes to insulin secretion by pancreatic β-cells

Liman, Emily R.

doi:10.4161/isl.2.5.12973

Cited by 13 publications

(7 citation statements)

References 28 publications

(32 reference statements)

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“…Trpm5 is expressed not only in the chemosensory cells but also in the mouse pancreatic β-cell line MIN6, pancreatic islets of Langerhans, and pancreatic β-cells ( Colsoul et al, 2010 , Nakagawa et al, 2009 , Oya et al, 2011 , Prawitt et al, 2003 , Yamamoto and Ishimaru, 2013 ). Trpm5 plays an important role in the regulation of GSIS from pancreatic β-cells via two major mechanisms: triggering and amplifying pathways ( Brixel et al, 2010 , Colsoul et al, 2010 , Liman, 2010 ). Trpm5 KO mice, like Skn-1 KO mice, gain significantly less body weight and fat mass and are more sensitive to insulin than WT mice when fed either a HFD or a high-carbohydrate diet ( Larsson et al, 2015 ).…”

Section: Discussionmentioning

confidence: 99%

Catecholamines Facilitate Fuel Expenditure and Protect Against Obesity via a Novel Network of the Gut-Brain Axis in Transcription Factor Skn-1-deficient Mice

et al. 2016

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Taste signals and nutrient stimuli sensed by the gastrointestinal tract are transmitted to the brain to regulate feeding behavior and energy homeostasis. This system is referred to as the gut-brain axis. Here we show that both brush cells and type II taste cells are eliminated in the gastrointestinal tract of transcription factor Skn-1 knockout (KO) mice. Despite unaltered food intake, Skn-1 KO mice have reduced body weight with lower body fat due to increased energy expenditure. In this model, 24-h urinary excretion of catecholamines was significantly elevated, accompanied by increased fatty acid β-oxidation and fuel dissipation in skeletal muscle and impaired insulin secretion driven by glucose. These results suggest the existence of brain-mediated energy homeostatic pathways originating from brush cells and type II taste cells in the gastrointestinal tract and ending in peripheral tissues, including the adrenal glands. The discovery of food-derived factors that regulate these cells may open new avenues the treatment of obesity and diabetes.Research ContextTaste signals and nutrient stimuli sensed by the gastrointestinal tract are transmitted to the brain to regulate feeding behavior and energy homeostasis along the gut-brain axis. We propose the concept that taste-receiving cells in the oral cavity and/or food-borne chemicals-receiving brush cells in the gut are involved in regulation of the body weight and adiposity via the brain. The discovery of food-derived factors that regulate these cells may open new avenues for the treatment of obesity and diabetes.

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Section: Discussionmentioning

confidence: 99%

Catecholamines Facilitate Fuel Expenditure and Protect Against Obesity via a Novel Network of the Gut-Brain Axis in Transcription Factor Skn-1-deficient Mice

et al. 2016

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“…Similarly, the presence of a voltage-dependent calcium channel subunit suggests that ␤-cell L-channels may be associated with FAs during glucose stimulation, allowing for localized increases in Ca 2ϩ to stimulate exocytosis; indeed, in ␤-cells, glucose-induced increases in intracellular Ca 2ϩ are more pronounced close to actin-rich filopodia (36). Intriguingly, the Ca 2ϩ transients seen at the leading edge of moving cells are mediated by TRPM7 (a member of the melastatin subfamily of transient receptor potential of cation channels that regulate multiple cell functions through Ca 2ϩ / Mg 2ϩ homeostasis) and generated through actomyosin contractility (144), while in islet cells both TRPM2 (127) and TRPM5 (69) have been shown to contribute toward insulin secretion, probably similarly driven by actin-myosin II tension at sites of exocytosis.…”

Section: Discovering More About the Skeleton In The Closet: New Evidementioning

confidence: 97%

The skeleton in the closet: actin cytoskeletal remodeling in β-cell function

Arous

Halban

2015

American Journal of Physiology-Endocrinology and Metabolism

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Over the last few decades, biomedical research has considered not only the function of single cells but also the importance of the physical environment within a whole tissue, including cell-cell and cell-extracellular matrix interactions. Cytoskeleton organization and focal adhesions are crucial sensors for cells that enable them to rapidly communicate with the physical extracellular environment in response to extracellular stimuli, ensuring proper function and adaptation. The involvement of the microtubular-microfilamentous cytoskeleton in secretion mechanisms was proposed almost 50 years ago, since when the evolution of ever more sensitive and sophisticated methods in microscopy and in cell and molecular biology have led us to become aware of the importance of cytoskeleton remodeling for cell shape regulation and its crucial link with signaling pathways leading to β-cell function. Emerging evidence suggests that dysfunction of cytoskeletal components or extracellular matrix modification influences a number of disorders through potential actin cytoskeleton disruption that could be involved in the initiation of multiple cellular functions. Perturbation of β-cell actin cytoskeleton remodeling could arise secondarily to islet inflammation and fibrosis, possibly accounting in part for impaired β-cell function in type 2 diabetes. This review focuses on the role of actin remodeling in insulin secretion mechanisms and its close relationship with focal adhesions and myosin II.

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“…The presence of CANs (Ca 2+ ‐activated non‐selective cation channels) has been described in human β ‐cells and related cell lines. Two TRP channels are candidates for these currents: TRPM4 and TRPM5 . TRPM4 deletion in mice, however, does not alter the results of a glucose tolerance test and glucose‐induced insulin release from the islets remains unchanged .…”

Section: Insulin Secretionmentioning

confidence: 99%

TRPM5 in the battle against diabetes and obesity

2017

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TRPM5 is a non-selective monovalent cation channel activated by increases in intracellular Ca . It has a distinct expression pattern: expression is detected in chemosensitive tissues from solitary chemosensory cells to the taste receptor cells and in pancreatic β-cells. The role of TRPM5 has been investigated with the use of knockout mouse models. Trpm5 mice have a lack of type II taste perception and show reduced glucose-induced insulin secretion. Expression levels of TRPM5 are reduced in obese, leptin-signalling-deficient mice, and mutations in TRPM5 have been associated with type II diabetes and metabolic syndrome. In this review, we aim to give an overview of the activation, selectivity, modulation and physiological roles of TRPM5.

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A TRP channel contributes to insulin secretion by pancreatic β-cells

Cited by 13 publications

References 28 publications

Catecholamines Facilitate Fuel Expenditure and Protect Against Obesity via a Novel Network of the Gut-Brain Axis in Transcription Factor Skn-1-deficient Mice

Catecholamines Facilitate Fuel Expenditure and Protect Against Obesity via a Novel Network of the Gut-Brain Axis in Transcription Factor Skn-1-deficient Mice

The skeleton in the closet: actin cytoskeletal remodeling in β-cell function

TRPM5 in the battle against diabetes and obesity

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