Effect of insulin on the production of prostacyclin and cell proliferation in cultured smooth muscle cells

Kazama, Y.; Noguchi, Takehiko; Kanemaru, Yoshifumi; Wakasugi, Masakiyo; Onaya, Toshimasa; Yoshida, Yasuhiko

doi:10.1016/0952-3278(89)90109-9

Cited by 5 publications

(3 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[48][49][50][51] It has been shown that the hyperinsulinemia and increased levels of insulin growth factors promote cell proliferation. 52 Interleukin-6, another important adipokine, also promotes cell proliferation in chronic inflammatory conditions. 53 The specific cytokines and the mechanisms by which neoplasia is promoted in the insulin-resistant state remain to be fully defined.…”

Section: Insulin Resistance and Chronic Inflammatory Statesmentioning

confidence: 99%

Hepatitis C and Nonalcoholic Fatty Liver Disease

Ramesh¹,

Sanyal²

2004

Semin Liver Dis

View full text Add to dashboard Cite

Hepatitis C virus (HCV) and nonalcoholic fatty liver disease (NAFLD) are the two most common causes of chronic liver disease in North America. NAFLD represents a spectrum of liver lesions that occur in individuals who either do not consume any alcohol or only consume alcohol in quantities generally considered not to be harmful to the liver. This spectrum consists of isolated hepatic macrovesicular steatosis at one end and nonalcoholic steatohepatitis (NASH) at the other. Hepatic steatosis is present in approximately 50% of the subjects with HCV. Genotype 3 is independently associated with hepatic steatosis. In those with genotype 1 infection, steatosis is associated with features of the metabolic syndrome. The presence of hepatic steatosis correlates with the stage of hepatic fibrosis in patients with HCV. This has been related to the presence of insulin resistance. Hepatic steatosis also adversely affects the virologic response rates to anti-HCV therapy. In this article, we will review the epidemiology of HCV and NAFLD, their impact on each other, and the course of the liver disease in individuals afflicted with both conditions.

show abstract

Section: Insulin Resistance and Chronic Inflammatory Statesmentioning

confidence: 99%

Hepatitis C and Nonalcoholic Fatty Liver Disease

Ramesh¹,

Sanyal²

2004

Semin Liver Dis

View full text Add to dashboard Cite

show abstract

“…C-peptide is cleaved from proinsulin and co-secreted with insulin in response to glucose stimulation. Insulin has been reported to accelerate SMC growth and promote atherosclerosis via the activation of p44/42 MAP kinases [24][25][26][27]. The proliferation of SMCs is one of the major pathological changes in atherosclerotic lesions occurring in the diabetic state [28].…”

Section: Discussionmentioning

confidence: 99%

Human proinsulin C-peptide prevents proliferation of rat aortic smooth muscle cells cultured in high-glucose conditions

et al. 2005

View full text Add to dashboard Cite

show abstract

“…C‐peptide can inhibit smooth muscle cells proliferation via suppressing the PDGF‐beta receptor and decreasing the phosphorylation of the p44/p42 MAP kinases pathway in a dose‐dependent manner (Kobayashi et al, 2005). In contrast, insulin upregulates VSMC proliferation, increases the expression of PDGF‐beta‐receptor, and promotes atherosclerotic lesions via the p42/44 MAP kinase pathway (Banskota et al, 1989; Huang et al, 2002; Kazama et al, 1989; Wang et al, 2003). It appears that C‐peptide and insulin, which are excreted in an equal amount from beta‐pancreatic cells, exert opposite effects.…”

Section: Anti‐atherogenic and Anti‐inflammatory Role Of C‐peptide In ...mentioning

confidence: 99%

C‐peptide in diabetes: A player in a dual hormone disorder?

Dakroub,

Dbouk,

Asfour

et al. 2024

Journal Cellular Physiology

View full text Add to dashboard Cite

C‐peptide, a byproduct of insulin synthesis believed to be biologically inert, is emerging as a multifunctional molecule. C‐peptide serves an anti‐inflammatory and anti‐atherogenic role in type 1 diabetes mellitus (T1DM) and early T2DM. C‐peptide protects endothelial cells by activating AMP‐activated protein kinase α, thus suppressing the activity of NAD(P)H oxidase activity and reducing reactive oxygen species (ROS) generation. It also prevents apoptosis by regulating hyperglycemia‐induced p53 upregulation and mitochondrial adaptor p66shc overactivation, as well as reducing caspase‐3 activity and promoting expression of B‐cell lymphoma‐2. Additionally, C‐peptide suppresses platelet‐derived growth factor (PDGF)‐beta receptor and p44/p42 mitogen‐activated protein (MAP) kinase phosphorylation to inhibit vascular smooth muscle cells (VSMC) proliferation. It also diminishes leukocyte adhesion by virtue of its capacity to abolish nuclear factor kappa B (NF‐kB) signaling, a major pro‐inflammatory cascade. Consequently, it is envisaged that supplementation of C‐peptide in T1DM might ameliorate or even prevent end‐organ damage. In marked contrast, C‐peptide increases monocyte recruitment and migration through phosphoinositide 3‐kinase (PI‐3 kinase)‐mediated pathways, induces lipid accumulation via peroxisome proliferator‐activated receptor γ upregulation, and stimulates VSMC proliferation and CD4+ lymphocyte migration through Src‐kinase and PI‐3K dependent pathways. Thus, it promotes atherosclerosis and microvascular damage in late T2DM. Indeed, C‐peptide is now contemplated as a potential biomarker for insulin resistance in T2DM and linked to increased coronary artery disease risk. This shift in the understanding of the pathophysiology of diabetes from being a single hormone deficiency to a dual hormone disorder warrants a careful consideration of the role of C‐peptide as a unique molecule with promising diagnostic, prognostic, and therapeutic applications.

show abstract

Effect of insulin on the production of prostacyclin and cell proliferation in cultured smooth muscle cells

Cited by 5 publications

References 25 publications

Hepatitis C and Nonalcoholic Fatty Liver Disease

Hepatitis C and Nonalcoholic Fatty Liver Disease

Human proinsulin C-peptide prevents proliferation of rat aortic smooth muscle cells cultured in high-glucose conditions

C‐peptide in diabetes: A player in a dual hormone disorder?

Contact Info

Product

Resources

About