Monoamines' role in islet cell function and type 2 diabetes risk

Roberts, Fiona Louise; Cataldo, Luis Rodrigo; Fex, Malin

doi:10.1016/j.molmed.2023.08.009

Cited by 6 publications

(3 citation statements)

References 118 publications

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“…A suggested explanation for the apparent discrepancy of these results is that the effect of melatonin on glucose regulation may be influenced by the timing of melatonin release or supplementation 201 . As melatonin inhibits insulin secretion in human and rodent islets in vitro, 202 meal consumption during periods of naturally increased melatonin concentrations may induce lower postprandial insulin secretion compared to meal intake during low melatonin levels 201 . In support, in a large randomized cross‐over trial with a population of patients with type 2 diabetes, late eating (1 h before bedtime) increased post‐OGTT glucose concentrations and decreased post‐OGTT insulin concentrations, compared to early eating (4 h before bedtime) 203 .…”

Section: Restoration Of Circadian Synchronymentioning

confidence: 99%

Circadian desynchrony and glucose metabolism

Speksnijder,

Bisschop,

Siegelaar

et al. 2024

Journal of Pineal Research

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The circadian timing system controls glucose metabolism in a time‐of‐day dependent manner. In mammals, the circadian timing system consists of the main central clock in the bilateral suprachiasmatic nucleus (SCN) of the anterior hypothalamus and subordinate clocks in peripheral tissues. The oscillations produced by these different clocks with a period of approximately 24‐h are generated by the transcriptional‐translational feedback loops of a set of core clock genes. Glucose homeostasis is one of the daily rhythms controlled by this circadian timing system. The central pacemaker in the SCN controls glucose homeostasis through its neural projections to hypothalamic hubs that are in control of feeding behavior and energy metabolism. Using hormones such as adrenal glucocorticoids and melatonin and the autonomic nervous system, the SCN modulates critical processes such as glucose production and insulin sensitivity. Peripheral clocks in tissues, such as the liver, muscle, and adipose tissue serve to enhance and sustain these SCN signals. In the optimal situation all these clocks are synchronized and aligned with behavior and the environmental light/dark cycle. A negative impact on glucose metabolism becomes apparent when the internal timing system becomes disturbed, also known as circadian desynchrony or circadian misalignment. Circadian desynchrony may occur at several levels, as the mistiming of light exposure or sleep will especially affect the central clock, whereas mistiming of food intake or physical activity will especially involve the peripheral clocks. In this review, we will summarize the literature investigating the impact of circadian desynchrony on glucose metabolism and how it may result in the development of insulin resistance. In addition, we will discuss potential strategies aimed at reinstating circadian synchrony to improve insulin sensitivity and contribute to the prevention of type 2 diabetes.

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Section: Restoration Of Circadian Synchronymentioning

confidence: 99%

Circadian desynchrony and glucose metabolism

Speksnijder,

Bisschop,

Siegelaar

et al. 2024

Journal of Pineal Research

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“…Treatment of enterochromaffin cells with various odorants known to bind those receptors (including eugenol, thymol, bourgeonal, and helional) elicited an increase in intracellular Ca 2+ levels and the secretion of serotonin [132]. In addition to regulating gut motility and the absorption of nutrients, serotonin may play a direct role in the stimulation of glucagon-like peptide-1 (GLP-1) release by enteroendocrine L cells, and it may even stimulate the release of insulin in the β-cells of the pancreatic islets [133,134].…”

Section: Regulation Of Incretin Secretionmentioning

confidence: 99%

Role of Ectopic Olfactory Receptors in the Regulation of the Cardiovascular–Kidney–Metabolic Axis

Beito,

Ashraf,

Odogwu

et al. 2024

Life

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Olfactory receptors (ORs) represent one of the largest yet least investigated families of G protein-coupled receptors in mammals. While initially believed to be functionally restricted to the detection and integration of odors at the olfactory epithelium, accumulating evidence points to a critical role for ectopically expressed ORs in the regulation of cellular homeostasis in extranasal tissues. This review aims to summarize the current state of knowledge on the expression and physiological functions of ectopic ORs in the cardiovascular system, kidneys, and primary metabolic organs and emphasizes how altered ectopic OR signaling in those tissues may impact cardiovascular–kidney–metabolic health.

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“…Glucose is the main regulator of insulin secretion but β cells also respond to other nutrients, including amino acids, 3,4 fatty acids, 5,6 and ketone bodies. 7,8 In addition, neurohormonal signals, such as acetylcholine, 9 serotonin, [10][11][12] dopamine, 10 y-aminobutyric acid (GABA), [13][14][15] melatonin, 16,17 glucagon, 18 somatostatin, 18 glucagon-like peptide 1 (GLP1) [19][20][21] and gastric insulinotropic peptide (GIP) 21 are important regulators of insulin secretion. Of note, most physiological potentiators of βcell hormone secretion act in a glucose-dependent manner as a safety mechanism to prevent hypoglycemia.…”

mentioning

confidence: 99%

Unique features of β‐cell metabolism are lost in type 2 diabetes

Muñoz,

Fex,

Moritz

et al. 2024

Acta Physiologica

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Pancreatic β cells play an essential role in the control of systemic glucose homeostasis as they sense blood glucose levels and respond by secreting insulin. Upon stimulating glucose uptake in insulin‐sensitive tissues post‐prandially, this anabolic hormone restores blood glucose levels to pre‐prandial levels. Maintaining physiological glucose levels thus relies on proper β‐cell function. To fulfill this highly specialized nutrient sensor role, β cells have evolved a unique genetic program that shapes its distinct cellular metabolism. In this review, the unique genetic and metabolic features of β cells will be outlined, including their alterations in type 2 diabetes (T2D). β cells selectively express a set of genes in a cell type‐specific manner; for instance, the glucose activating hexokinase IV enzyme or Glucokinase (GCK), whereas other genes are selectively “disallowed”, including lactate dehydrogenase A (LDHA) and monocarboxylate transporter 1 (MCT1). This selective gene program equips β cells with a unique metabolic apparatus to ensure that nutrient metabolism is coupled to appropriate insulin secretion, thereby avoiding hyperglycemia, as well as life‐threatening hypoglycemia. Unlike most cell types, β cells exhibit specialized bioenergetic features, including supply‐driven rather than demand‐driven metabolism and a high basal mitochondrial proton leak respiration. The understanding of these unique genetically programmed metabolic features and their alterations that lead to β‐cell dysfunction is crucial for a comprehensive understanding of T2D pathophysiology and the development of innovative therapeutic approaches for T2D patients.

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Monoamines' role in islet cell function and type 2 diabetes risk

Cited by 6 publications

References 118 publications

Circadian desynchrony and glucose metabolism

Circadian desynchrony and glucose metabolism

Role of Ectopic Olfactory Receptors in the Regulation of the Cardiovascular–Kidney–Metabolic Axis

Unique features of β‐cell metabolism are lost in type 2 diabetes

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