The Effects of Insulin-Like Growth Factor-1 on Plasminogen Activator Inhibitor-1 Synthesis and Secretion: Results from In Vitro and In Vivo Studies

Padayatty, Sebastian J.; Orme, Stephen M.; Zenobi, P D; Stickland, M. H.; Belchetz, P. E.; Grant, Peter J.

doi:10.1055/s-0038-1649716

Cited by 36 publications

(26 citation statements)

References 26 publications

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“…IGF-I, which acts as a mediator of the GH, and good nutritional status of the animals also help to decrease PA, probably through the stimulation of PAI (Padayatty et al, 1993). It is well known that administration of exogenous GH to sheep (Baldi et al, 1997;Baldi, 1999;Chiofalo et al, 1999), cows (Politis et al, 1990), and goats (Baldi et al, 2002) increases milk yield and lactation persistency and reduces plasmin activity, probably through its mediator IGF-I.…”

Section: Other Factors: the Role Of The Plasminplasminogen Systemmentioning

confidence: 99%

Non-nutritional factors affecting lactation persistency in dairy ewes: a review

Pulina

Nudda

Macciotta

et al. 2007

Italian Journal of Animal Science

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Milk production is largely related to the shape of the lactation curve. Key elements of the lactation pattern are peak yield, which is the maximum daily yield reached during lactation, and lactation persistency, which is the medium rate of milk yield decrease after the lactation peak. The ideal lactation curve should have a reasonably high peak and a flat trend afterwards. A more persistent lactation is desirable because it is related to better animal health and reduction of feeding costs. Effective strategies to improve lactation persistency require a deep understanding of the main factors that affect this trait, including genetics, hormonal status and administration, udder morphology, seasonal changes, management, animal health (e.g. mastitis), stress and nutrition. This review covers the effects of non-nutritional factors on lactation persistency in dairy sheep.

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Section: Other Factors: the Role Of The Plasminplasminogen Systemmentioning

confidence: 99%

Non-nutritional factors affecting lactation persistency in dairy ewes: a review

Pulina

Nudda

Macciotta

et al. 2007

Italian Journal of Animal Science

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“…Lipoprotein(a) (Lp(a)), an important risk factor for CAD, also improved after IGF-I treatment (89). The risk of coronary thrombosis (as measured by plasminogen activator inhibitor-1 and fibrinogen levels) also improved after IGF-I treatment (111). Moreover, IGF-I treatment decreases obesity and improves body composition of type 2 diabetics (109,112).…”

Section: Diabetic Cardiomyopathymentioning

confidence: 99%

The role of IGF-I in the development of cardiovascular disease in type 2 diabetes mellitus: is prevention possible?

Janssen

Lamberts

2002

European Journal of Endocrinology

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The incidence of peripheral, cerebro-and cardiovascular disease (CVD) in patients with type 2 diabetes mellitus is approximately twice as high as in the non-diabetic population. Conventional cardiovascular risk factors such as plasma lipids, lipoproteins and hypertension only partially explain this excessive risk of developing atherosclerosis and CVD. Meta-analysis of studies performed in nondiabetic populations indicates that the risk of CVD increases continuously with glucose levels above 4.2 mmol/l. The glucose hypothesis suggests that treatment which normalizes glucose levels prevents or delays the long-term complications of diabetes mellitus. However, the outcome of the UK Prospective Diabetes Study demonstrates that glucose control does not completely prevent CVD. In healthy subjects, serum IGF-I levels peak in early adulthood, after which they gradually decrease with increasing age. Several observations suggest that there is a premature and progressive agerelated decline in serum IGF-I bioactivity in type 2 diabetics, which eventually results in a (relative) IGF-I deficiency. In type 2 diabetics, close relationships have been demonstrated between glycaemic control and serum IGF-I levels, with worse control being associated with lower IGF-I levels. Several studies (in non-diabetics) suggest that lowered circulating IGF-I levels account for a poor outcome of CVD. We previously observed in a population-based study that a genetically determined lowered IGF-I expression increases the risk of myocardial infarction with type 2 diabetes. This genetic approach overcomes the problem that cross-sectional studies cannot distinguish whether changes in IGF-I levels are a cause or a consequence of a disease. IGF-I is an important metabolic regulatory hormone. In addition, IGF-I suppresses myocardial apoptosis and improves myocardial function in various models of experimental cardiomyopathy. Compared with other growth factors, the 'survival' effect of IGF-I on myocardium seems rather unique. Therefore, we hypothesize that the premature and progressive decline in serum IGF-I bioactivity in ageing patients with type 2 diabetics is an important pathophysiological abnormality. It contributes not only to elevated glucose and lipid levels, but also to the progression and the poor outcome of CVD. If this hypothesis is proven to be right, treatment with IGF-I as an adjunct to insulin offers great potential and might not only improve metabolic control but also reduce the incidence and prevalence of CVD in type 2 diabetes patients. However, there is as yet no experimental evidence that long-term (replacement) treatment with IGF-I prevents, delays or reduces CVD in type 2 diabetes patients. Clinical trials are necessary to prove that long-term IGF-I treatment, preferably in the form of a bettertolerated IGF-I/IGF-binding protein-3 complex, improves the overall cardiovascular risk in type 2 diabetes.

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“…Selective elimination of IGF-1 from serum or synovial fluid with neutralizing antibodies results in a distinct decrease in cartilage proteoglycan synthesis and enhanced proteoglycan breakdown (Schalkwijk et al, 1989a). IGF-1 seems to inhibit production and release of proteases or protease activators, although evidence is not yet conclusive (Ballard et al, 1986;Chandrasekhar et al, 1992;Padayatty et al, 1993).…”

Section: Effects Of Igf On Proteoglycan Metabolism In Cartilagementioning

confidence: 99%

Articular cartilage destruction in experimental inflammatory arthritis: insulin-like growth factor-1 regulation of proteoglycan metabolism in chrondrocytes

et al. 1996

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Rheumatoid arthritis, a disease of unknown aetiology, is characterized by joint inflammation and, in its later stages, cartilage destruction. Inflammatory mediators may exert not only suppression of matrix synthesis but also cartilage degradation, which eventually leads to severe cartilage depletion. Systemically and locally produced growth factors and hormones regulate cartilage metabolism. Alterations in levels of these factors or in their activity can influence the pathogenesis of articular cartilage destruction in arthritic joints. The main topic of the present review is the role of the anabolic factor insulin-like growth factor-1 in the regulation of chondrocyte metabolic functions in normal and in diseased cartilage. This is the most important growth factor that balances chondrocytes proteoglycan synthesis and catabolism to maintain a functional cartilage matrix. A brief overview of how chondrocytes keep the cartilage matrix intact, and how catabolic and anabolic factors are thought to be involved in pathological cartilage destruction precedes the review of the role of this growth factor in proteoglycan metabolism in cartilage.

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The Effects of Insulin-Like Growth Factor-1 on Plasminogen Activator Inhibitor-1 Synthesis and Secretion: Results from In Vitro and In Vivo Studies

Cited by 36 publications

References 26 publications

Non-nutritional factors affecting lactation persistency in dairy ewes: a review

Non-nutritional factors affecting lactation persistency in dairy ewes: a review

The role of IGF-I in the development of cardiovascular disease in type 2 diabetes mellitus: is prevention possible?

Articular cartilage destruction in experimental inflammatory arthritis: insulin-like growth factor-1 regulation of proteoglycan metabolism in chrondrocytes

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