Glucosamine enhances body weight gain and reduces insulin response in mice fed chow diet but mitigates obesity, insulin resistance and impaired glucose tolerance in mice high-fat diet.

@article{Hwang2015GlucosamineEB,
  title={Glucosamine enhances body weight gain and reduces insulin response in mice fed chow diet but mitigates obesity, insulin resistance and impaired glucose tolerance in mice high-fat diet.},
  author={Ji‐Sun Hwang and Jiwon Park and Moonsuk Nam and Hyeongjin Cho and Inn-Oc Han},
  journal={Metabolism: clinical and experimental},
  year={2015},
  volume={64 3},
  pages={
          368-79
        }
}

Figures from this paper

Chitosan Oligosaccharide Alleviates Abnormal Glucose Metabolism without Inhibition of Hepatic Lipid Accumulation in a High-Fat Diet/Streptozotocin-Induced Diabetic Rat Model

The results suggest that COS may possess a potential for alleviating abnormal glucose metabolism in diabetic rats through the inhibition of hepatic gluconeogenesis and lipid peroxidation and renal SGLT2 expression.

Glucosamine Ameliorates Symptoms of High-Fat Diet-Fed Mice by Reversing Imbalanced Gut Microbiota

It was demonstrated that GlcN not only inhibited the inflammatory responses of colon and white adipose tissues, but also improved the intestinal barrier damage of HFD-fed mice and provided a theoretical basis for the potential application of Glcn to glucolipid metabolism disorder through the regulation of gut microbiota.

Chitosan Oligosaccharides Improve Glucolipid Metabolism Disorder in Liver by Suppression of Obesity-Related Inflammation and Restoration of Peroxisome Proliferator-Activated Receptor Gamma (PPARγ)

COS pretreatment significantly reversed the downregulation of PPARγ at transcriptional and translational levels in both PA-induced HepG2 cells and liver tissues of HFD-fed mice, indicating a novel application of COS in preventing and treating glucolipid metabolism-related diseases.

Pear pomace ethanol extract improves insulin resistance through enhancement of insulin signaling pathway without lipid accumulation

It is shown that PPE improves glucose uptake in 3T3-L1 cells and insulin sensitivity in mice fed a HFD through stimulation of the insulin signaling pathway and PPE-induced improvement of insulin sensitivity was not accompanied with lipid accumulation.

An Avocado Extract Enriched in Mannoheptulose Prevents the Negative Effects of a High-Fat Diet in Mice

Beyond generating further interest in the health benefits of avocados, these results draw further new attention to the effects of this rare sugar, MH, as a botanical intervention for preventing obesity.

Lipopolysaccharide (LPS)-stimulated iNOS Induction Is Increased by Glucosamine under Normal Glucose Conditions but Is Inhibited by Glucosamine under High Glucose Conditions in Macrophage Cells*

The results suggest that GlcN regulates inflammation by sensing energy states of normal and fuel excess by suppressing LPS-induced up-regulation of COX-2, IL-6, and TNF-α mRNAs under 25 mm glucose conditions and blocking transcription with actinomycin D increases stability of L PS-induced iNOS mRNA under normal glucose conditions.

A Mouse Model of Metabolic Syndrome: Insulin Resistance, Fatty Liver and Non-Alcoholic Fatty Pancreas Disease (NAFPD) in C57BL/6 Mice Fed a High Fat Diet

C57BL/6 mice fed a high-fat diet develop features of NAFPD, and the HFC mice showed larger pancreatic islet size and significantly greater alpha and beta-cell immunodensities than SC mice.

Glucosamine induces insulin resistance in vivo by affecting GLUT 4 translocation in skeletal muscle. Implications for glucose toxicity.

Glucosamine is a potent inducer of insulin resistance in vivo by causing (at least in part) a defect intrinsic to GLUT 4 translocation and/or trafficking and a potential role for Glmn to cause glucose-induced insulin resistance (glucose toxicity).

In vivo effects of glucosamine on insulin secretion and insulin sensitivity in the rat: Possible relevance to the maladaptive responses to chronic hyperglycaemia

An increase in hexosamine metabolism in vivo inhibits glucose-induced insulin secretion, and reduces insulin stimulation of both glycolysis and glycogen synthesis, thereby mimicking in normal rats the major alterations due to glucose toxicity in diabetes.

In vivo glucosamine infusion induces insulin resistance in normoglycemic but not in hyperglycemic conscious rats.

The lack of additive effects of GlcN and chronic hyperglycemia (experimental diabetes) provides support for the hypothesis that increased flux through the Glcn pathway in skeletal muscle may play an important role in glucose-induced insulin resistance in vivo.

Increased hexosamine pathway flux and high fat feeding are not additive in inducing insulin resistance: evidence for a shared pathway

It is reported here that hexosamine-induced insulin resistance is not additive with that induced by high fat feeding, which is consistent with a shared nutrient sensing pathway for high fat and carbohydrate fluxes and a common pathway by which glucose and lipids induce insulin resistance.

Role of the glucosamine pathway in fat-induced insulin resistance.

The hypothesis that increased FFA availability induces skeletal muscle insulin resistance by increasing the flux of fructose-6-phosphate into the hexosamine pathway is supported.

Development of insulin resistance and obesity in mice overexpressing cellular glutathione peroxidase

  • J. McClungC. Roneker X. Lei
  • Biology, Medicine
    Proceedings of the National Academy of Sciences of the United States of America
  • 2004
The development of insulin resistance in mammals with elevated expression of an antioxidant enzyme is reported and it is suggested that increased GPX1 activity may interfere with insulin function by overquenching intracellular reactive oxygen species required for insulin sensitizing.

Signaling pathways in insulin action: molecular targets of insulin resistance.

The regulation of glucose transport as the rate-limiting step in glucose utilization and storage is focused on.