Characterization of Insulin Receptors in Chicken Kidneys: Effect of Nutritional Status

Bisbis, Selma; Derouet, Michel; Simon, Jean

doi:10.1006/gcen.1994.1157

Cited by 16 publications

(5 citation statements)

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“…For example, mRNA and protein levels of rat intestinal InR increase up to 230% in fasting conditions, and these effects are fully reversed by refeeding (Ziegler et al 1995). Similar observations have been made in other organisms (Bisbis et al 1994;Dupont et al 1998). These effects indicate a nutritional influence on the abundance of the InR.…”

Section: Foxo1 Regulates Inr Transcriptionsupporting

confidence: 74%

Transcriptional feedback control of insulin receptor by dFOXO/FOXO1

Puig¹,

Tjian²

2005

Genes Dev.

324

265

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The insulin signaling pathway, which is conserved in evolution from flies to humans, evolved to allow a fast response to changes in nutrient availability while keeping glucose concentration constant in serum. Here we show that, both in Drosophila and mammals, insulin receptor (InR) represses its own synthesis by a feedback mechanism directed by the transcription factor dFOXO/FOXO1. In Drosophila, dFOXO is responsible for activating transcription of dInR, and nutritional conditions can modulate this effect. Starvation up-regulates mRNA of dInR in wild-type but not dFOXO-deficient flies. Importantly, FOXO1 acts in mammalian cells like its Drosophila counterpart, up-regulating the InR mRNA level upon fasting. Mammalian cells up-regulate the InR mRNA in the absence of serum, conditions that induce the dephosphorylation and activation of FOXO1. Interestingly, insulin is able to reverse this effect. Therefore, dFOXO/FOXO1 acts as an insulin sensor to activate insulin signaling, allowing a fast response to the hormone after each meal. Our results reveal a key feedback control mechanism for dFOXO/FOXO1 in regulating metabolism and insulin signaling.

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Section: Foxo1 Regulates Inr Transcriptionsupporting

confidence: 74%

Transcriptional feedback control of insulin receptor by dFOXO/FOXO1

Puig¹,

Tjian²

2005

Genes Dev.

324

265

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“…In the renal medulla, radioligand binding was detected primarily in longitudinal structures crossing the outer portion, presumably corresponding to interlobar vessels, and the inner portion, presumably corresponding to hilar fat. The same distribution of renal insulin receptors was reported in the chicken kidney which was shown to be upregulated by fasting [ 32 ]. In these experiments, the precise nature of the receptors identified by radiolabeled insulin was not entirely certain due to the possibility of nonspecific binding to other receptors that can be detected in the kidney, such as those for the insulin growth factor.…”

Section: Insulin and The Kidneysupporting

confidence: 66%

Insulin Resistance and High Blood Pressure: Mechanistic Insight on the Role of the Kidney

et al. 2022

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The metabolic effects of insulin predominate in skeletal muscle, fat, and liver where the hormone binds to its receptor, thereby priming a series of cell-specific and biochemically diverse intracellular mechanisms. In the presence of a good secretory reserve in the pancreatic islets, a decrease in insulin sensitivity in the metabolic target tissues leads to compensatory hyperinsulinemia. A large body of evidence obtained in clinical and experimental studies indicates that insulin resistance and the related hyperinsulinemia are causally involved in some forms of arterial hypertension. Much of this involvement can be ascribed to the impact of insulin on renal sodium transport, although additional mechanisms might be involved. Solid evidence indicates that insulin causes sodium and water retention, and both endogenous and exogenous hyperinsulinemia have been correlated to increased blood pressure. Although important information was gathered on the cellular mechanisms that are triggered by insulin in metabolic tissues and on their abnormalities, knowledge of the insulin-related mechanisms possibly involved in blood pressure regulation is limited. In this review, we summarize the current understanding of the cellular mechanisms that are involved in the pro-hypertensive actions of insulin, focusing on the contribution of insulin to the renal regulation of sodium balance and body fluids.

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“…Moreover, an association between insulin resistance and albuminuria has been reported in nondiabetic individuals in a recent RISC study . It is quite possible that reduced IR signaling in the kidney in the fasting state may affect tubular uptake of albumin . In the kidneys, the PT is the major renal tubular site for albumin reabsorption (up to 71%) .…”

Section: Discussionmentioning

confidence: 98%

“…7 It is quite possible that reduced IR signaling in the kidney in the fasting state may affect tubular uptake of albumin. 23 In the kidneys, the PT is the major renal tubular site for albumin reabsorption (up to 71%). 24 Receptor-mediated endocytosis involves proteins, such as megalin and cubulin, the multiligand receptors present on the brush border epithelium of PT cells, as the central players in the absorption process.…”

Section: Discussionmentioning

confidence: 99%

Deletion of insulin receptor in the proximal tubule and fasting augment albumin excretion

Kumari

Sharma

Pandey

et al. 2019

J of Cellular Biochemistry

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The contribution of proximal tubules (PT) to albumin uptake is now well recognized, however, its regulation is understudied area. There are reports suggesting that insulin resistance is associated with the development of albuminuria in nondiabetic individuals. We have previously reported reduced insulin receptor (IR) expression in renal-tubular-epithelial cells, including PT in various models of insulin resistance. However, the effect of a physiological fall in insulin levels and the role for IR in PT in tubular albumin uptake is not clear. To address these gaps in our understanding, we estimated urine excretion and renal uptake of albumin in fasted and fed C57Bl/6 mice injected with fluorescein isothiocyanate (FITC)-

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Characterization of Insulin Receptors in Chicken Kidneys: Effect of Nutritional Status

Cited by 16 publications

References 0 publications

Transcriptional feedback control of insulin receptor by dFOXO/FOXO1

Transcriptional feedback control of insulin receptor by dFOXO/FOXO1

Insulin Resistance and High Blood Pressure: Mechanistic Insight on the Role of the Kidney

Deletion of insulin receptor in the proximal tubule and fasting augment albumin excretion

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