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insulin resistance/phosphatase
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PHLPP phosphatases as a therapeutic target in insulin resistance-related diseases.
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BACKGROUND
Pleckstrin homology domain leucine-rich repeat protein phosphatases (PHLPPs), originally identified as Akt kinase hydrophobic motif specific phosphatases, have subsequently been shown to regulate several molecules recurring within the insulin signaling pathway. This observation suggests
A novel protein tyrosine phosphatase 1 B inhibitor-geranylated flavonoid from mulberry leaves ameliorates insulin resistance
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Mulberry leaf is a common vegetable with a variety of beneficial effects, such as hypoglycemic activity. However, the underlying mechanism of its hypoglycemic effect have not been fully revealed. In this study, two flavonoid derivatives were isolated from mulberry leaves, a new geranylated flavonoid
Insulin resistance and the transcription of the glucose-6-phosphatase gene in newborn dogs.
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In the present report changes in the mRNA level of glucose-6-phosphatase (G6Pase; EC 3.1.39) in newborn and adult dogs in vivo were studied to further test the hypotheses that neonatal hyperglycemia may be due to unsuppressed gluconeogenesis by insulin and that the antidiabetic role of insulin-like
Role of glucose-6 phosphatase, glucokinase, and glucose-6 phosphate in liver insulin resistance and its correction by metformin.
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We investigated the role of glucose-6 phosphatase (Glc6Pase), glucokinase (GK), and glucose-6 phosphate (Glc6P) in liver insulin resistance, an early characteristic of type 2 diabetes, and its correction by metformin. We determined hepatic glucose production (HGP) by tracer dilution, and enzyme
Inhibition of Src homology 2 domain-containing phosphatase 1 increases insulin sensitivity in high-fat diet-induced insulin-resistant mice.
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Insulin resistance plays a crucial role in the development of type 2 diabetes. Insulin receptor signalling is antagonized and tightly controlled by protein tyrosine phosphatases (PTPs). However, the precise role of the PTP src homology 2 domain-containing phosphatase 1 (SHP-1) in insulin resistance
Effects of exercise on insulin sensitivity, inflammatory cytokines, and serum tartrate-resistant acid phosphatase 5a in obese Chinese male adolescents.
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The benefits of exercise on glucose metabolism, inflammation, and serum tartrate-resistant acid phosphatase 5a (TRACP 5a) protein levels in Chinese male adolescents have not been extensively analyzed. Therefore, we examined the effects of a 12-week exercise program on weight, adiposity, insulin
Silymarin induces insulin resistance through an increase of phosphatase and tensin homolog in Wistar rats.
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OBJECTIVE
Phosphatase and tensin homolog (PTEN) is a phosphoinositide phosphatase that regulates crucial cellular functions, including insulin signaling, lipid and glucose metabolism, as well as survival and apoptosis. Silymarin is the active ingredient in milk thistle and exerts numerous effects
A novel protein tyrosine phosphatase 1B inhibitor with therapeutic potential for insulin resistance.
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Insulin-sensitizing drugs are currently limited, and identifying new candidates is a challenge. Protein tyrosine phosphatase 1B (PTP1B) negatively regulates insulin signalling, and its inhibition is anticipated to improve insulin resistance. Here, the pharmacological properties of CX08005, a novel
Evidence for sex-specific associations between variation in acid phosphatase locus 1 (ACP1) and insulin sensitivity in Mexican-Americans.
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BACKGROUND
Acid phosphatase locus 1 (ACP1) is a low molecular weight tyrosine phosphatase that has been shown to be an important regulator of insulin receptor signaling.
OBJECTIVE
We tested whether variation in ACP1 is associated with type 2 diabetes-related traits in 1035 individuals in 339
Molecular mechanism of angiotensin II-induced insulin resistance in aortic vascular smooth muscle cells: roles of Protein Tyrosine Phosphatase-1B.
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Insulin resistance is an underlying mechanism of type 2 diabetes and its vascular complications. Recent evidence suggests that crosstalk between angiotensin II (Ang II) and the insulin signaling in vascular smooth muscle cell (VSMC) may contribute to cellular insulin resistance. We hypothesized that
Leptin increases hepatic insulin sensitivity and protein tyrosine phosphatase 1B expression.
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Leptin has been shown to improve insulin sensitivity and glucose metabolism in obese diabetic ob/ob mice, yet the mechanisms remain poorly defined. We found that 2 d of leptin treatment improved fasting but not postprandial glucose homeostasis, suggesting enhanced hepatic insulin sensitivity.
Protein-tyrosine phosphatase 1B deficiency reduces insulin resistance and the diabetic phenotype in mice with polygenic insulin resistance.
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Mice heterozygous for insulin receptor (IR) and IR substrate (IRS)-1 deficiency provide a model of polygenic type 2 diabetes in which early-onset, genetically programmed insulin resistance leads to diabetes. Protein-tyrosine phosphatase 1B (PTP1B) dephosphorylates tyrosine residues in IR and
Protein-tyrosine phosphatases are involved in interferon resistance associated with insulin resistance in HepG2 cells and obese mice.
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Insulin resistance is a risk factor for non-response to interferon/ribavirin therapy in patients with chronic hepatitis C. The aim of this study was to determine the role played by protein-tyrosine phosphatases (PTPs) in the absence of interferon-α (IFNα) response associated with insulin resistance.
Alterations in specific protein-tyrosine phosphatases accompany insulin resistance of streptozotocin diabetes.
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To test whether protein tyrosine phosphatases (PTPases) may play a role in the insulin resistance of insulinopenic diabetes, we assessed PTPase activity as well as the protein and mRNA abundance of three major candidate PTPases in subcellular fractions of liver and skeletal muscle of
Involvement of protein tyrosine phosphatases and inflammation in hypothalamic insulin resistance associated with ageing: effect of caloric restriction.
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Aged Wistar rats present central insulin resistance associated with ageing. Several steps of the insulin signaling pathway have been described to be impaired in aged rats at hypothalamic level. In the present article we have explored possible alterations in protein tyrosine phosphatases (PTPs)
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