Exercise profoundly influences glycemic control by enhancing muscle insulin sensitivity, thus promoting glucometabolic health. While prior glycogen breakdown so far has been deemed integral for muscle insulin sensitivity to be potentiated by exercise, the mechanisms underlying this phenomenon remain enigmatic. We have combined original data from 13 of our studies that investigated insulin action in skeletal muscle either under rested conditions or following a bout of one-legged knee extensor exercise in healthy young male individuals (n = 106). Insulin-stimulated glucose uptake was potentiated and occurred substantially faster in the prior contracted muscles. In this otherwise homogenous group of individuals, a remarkable biological diversity in the glucometabolic responses to insulin is apparent both in skeletal muscle and at the whole-body level. In contrast to the prevailing concept, our analyses reveal that insulin-stimulated muscle glucose uptake and the potentiation thereof by exercise are not associated with muscle glycogen synthase activity, muscle glycogen content, or degree of glycogen utilization during the preceding exercise bout. Our data further suggest that the phenomenon of improved insulin sensitivity in prior contracted muscle is not regulated in a homeostatic feedback manner from glycogen. Instead, we put forward the idea that this phenomenon is regulated by cellular allostatic mechanisms that elevate the muscle glycogen storage set point and enhance insulin sensitivity to promote the uptake of glucose toward faster glycogen resynthesis without development of glucose overload/toxicity or feedback inhibition.
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http://dx.doi.org/10.2337/db22-0015 | DOI Listing |
Endocrinol Diabetes Metab
January 2025
Universidad Autónoma de Madrid, Department of Endocrinology and Nutrition, Hospital Universitario de La Princesa, Instituto de Investigación Sanitaria de La Princesa, Madrid, Spain.
Purpose: To investigate the impact of clinical and socio-economic factors on glycaemic control and construct statistical models to predict optimal glycaemic control (OGC) after implementing intermittently scanned continuous glucose monitoring (isCGM) systems.
Methods: This retrospective study included 1072 type 1 diabetes patients (49.0% female) from three centres using isCGM systems.
Genes Dis
March 2025
Department of Genetics and Genome Sciences, Case Western Reserve University, Cleveland, OH 44106, USA.
Phosphoinositide 3-kinases (PI3Ks) are heterodimers consisting of a p110 catalytic subunit and a p85 regulatory subunit. The gene, which encodes the p110α, is the most frequently mutated oncogene in cancer. Oncogenic mutations activate the PI3K pathway, promote tumor initiation and development, and mediate resistance to anti-tumor treatments, making the mutant p110α an excellent target for cancer therapy.
View Article and Find Full Text PDFJHEP Rep
January 2025
Department of Pharmacology, Wuhan University TaiKang Medical School (School of Basic Medical Sciences), Wuhan 430071, China.
Background & Aims: Hepatic immune imbalance is crucial for driving metabolic dysfunction-associated steatotic liver disease (MASLD) progression. However, the role of hepatic regulatory T cells (Tregs) in MASLD initiation and the mechanisms responsible for their change are not completely understood.
Methods: A mouse model subjected to a short-term high-fat diet (HFD) to mimic early steatosis, along with liver biopsy samples from patients with simple steatosis, and macrophage-specific Notch1-knockout mice (Notch1), were used to investigate the role of Tregs in early MASLD and the effect of hepatic macrophage Notch1 signaling on Treg frequency.
JCEM Case Rep
January 2025
Department of Paediatric Endocrinology, Kandang Kerbau Women's and Children's Hospital, 229899 Singapore.
Maturity-onset diabetes of the young (MODY) represents 1% to 5% of patients with diabetes mellitus (DM), and numerous genes associated with MODY have been identified. While mutations of the insulin gene () are known to cause permanent neonatal DM, rare disease-causing variants have also been found in MODY. These patients demonstrate variable clinical phenotypes-from milder forms requiring lifestyle or oral agent interventions to severe forms requiring lifelong insulin.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
December 2024
Tianjin Union Medical Center, Tianjin Medical University, Tianjin, China.
Background: Postmenopausal women represent the demographic increasingly susceptible to cardiovascular and metabolic diseases. Elevated levels of remnant cholesterol (RC) have been implicated in atherosclerosis and insulin resistance.
Methods: This study aimed to investigate the relationship between RC and the prevalence of coronary heart disease (CHD), diabetes, and CHD combined with diabetes in a nationally representative sample of US postmenopausal women using data from the National Health and Nutrition Examination Survey (NHANES) 2007-2018.
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