Homogenization-dependent responses of acid-soluble and acid-insoluble glycogen to exercise and refeeding in human muscles

Barnes, Phillip D.; Singh, Anish; Fournier, Paul A.

doi:10.1016/j.metabol.2009.06.016

Cited by 6 publications

(3 citation statements)

References 45 publications

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“…This idea is supported by studies reporting that the acid-insoluble glycogen fraction is more metabolically active (10) and has lower average external chain lengths (11). Interestingly, the amount of glycogen acid-soluble fraction has been reported to be more responsive to fasting/feeding and exercise/re-feeding cycles (23,78). These results may seem contradictory; yet, they can be rationalized by the proposed model.…”

Section: Intracellular Compartmentalization and Dynamics Of A Glycogementioning

confidence: 96%

The dynamic life of the glycogen granule

Prats

Graham

Shearer

2018

Journal of Biological Chemistry

153

117

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Glycogen, the primary storage form of glucose, is a rapid and accessible form of energy that can be supplied to tissues on demand. Each glycogen granule, or "glycosome," is considered an independent metabolic unit composed of a highly branched polysaccharide and various proteins involved in its metabolism. In this Minireview, we review the literature to follow the dynamic life of a glycogen granule in a multicompartmentalized system, the cell, and how and where glycogen granules appear and the factors governing its degradation. A better understanding of the importance of cellular compartmentalization as a regulator of glycogen metabolism is needed to unravel its role in brain energetics.

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Section: Intracellular Compartmentalization and Dynamics Of A Glycogementioning

confidence: 96%

The dynamic life of the glycogen granule

Prats

Graham

Shearer

2018

Journal of Biological Chemistry

153

117

View full text Add to dashboard Cite

show abstract

“…It has been under debate whether the labile glycogen corresponds to larger glycogen particles (with molecular mass of ~10 7 Da) and the stabile glycogen to smaller protein (glycogenin)‐binding particles (with mass of ~4 × 10 5 Da), and about their actual physiological meanings . However, there is an agreement on the existence of glycogen particles with different solubility in TCA, and that changes occur in the ratio of the labile and stabile structures (LF/SF ratio) in different physiological and pathological conditions . In a physiological glycogen synthesis, when fasted animals are administered with glucose, the stabile fraction is initially quickly increased, but then the labile fraction increases being responsible for the actual glycogen accumulation .…”

Section: Introductionmentioning

confidence: 99%

“…[13][14][15][16] However, there is an agreement on the existence of glycogen particles with different solubility in TCA, and that changes occur in the ratio of the labile and stabile structures (LF/SF ratio) in different physiological and pathological conditions. 17 In a physiological glycogen synthesis, when fasted animals are administered with glucose, the stabile fraction is initially quickly increased, but then the labile fraction increases being responsible for the actual glycogen accumulation. 18 In contrast, in a pathologic situation of liver cirrhosis, the stabile fraction is especially increased and the ratio of LF/SF decreased, suggesting a more stable increase in glycogen.…”

Section: Introductionmentioning

confidence: 99%

Metformin normalizes the structural changes in glycogen preceding prediabetes in mice overexpressing neuropeptide Y in noradrenergic neurons

Ailanen

Bezborodkina

Virtanen

et al. 2018

Pharmacology Res & Perspec

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Hepatic insulin resistance and increased gluconeogenesis are known therapeutic targets of metformin, but the role of hepatic glycogen in the pathogenesis of diabetes is less clear. Mouse model of neuropeptide Y (NPY) overexpression in noradrenergic neurons (OE‐NPYD βH) with a phenotype of late onset obesity, hepatosteatosis, and prediabetes was used to study early changes in glycogen structure and metabolism preceding prediabetes. Furthermore, the effect of the anti‐hyperglycemic agent, metformin (300 mg/kg/day/4 weeks in drinking water), was assessed on changes in glycogen metabolism, body weight, fat mass, and glucose tolerance. Glycogen structure was characterized by cytofluorometric analysis in isolated hepatocytes and mRNA expression of key enzymes by qPCR. OE‐NPYD βH mice displayed decreased labile glycogen fraction relative to stabile fraction (the intermediate form of glycogen) suggesting enhanced glycogen cycling. This was supported by decreased filling of glucose residues in the 10th outer tier of the glycogen molecule, which suggests accelerated glycogen phosphorylation. Metformin reduced fat mass gain in both genotypes, but glucose tolerance was improved mostly in wild‐type mice. However, metformin inhibited glycogen accumulation and normalized the ratio between glycogen structures in OE‐NPYD βH mice indicating decreased glycogen synthesis. Furthermore, the presence of glucose residues in the 11th tier together with decreased glycogen phosphorylase expression suggested inhibition of glycogen degradation. In conclusion, structural changes in glycogen of OE‐NPYD βH mice point to increased glycogen metabolism, which may predispose them to prediabetes. Metformin treatment normalizes these changes and suppresses both glycogen synthesis and phosphorylation, which may contribute to its preventive effect on the onset of diabetes.

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