Figure 1 Role of the kidney in glucose homeostasis

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Mindarie Senior College 3A/3B HUMAN BIOLOGICAL SCIENCE HOMEOSTASIS HOMEOSTATIC MECHANISMS.

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Figure 1 Disruption of phosphate homeostasis in chronic kidney disease (CKD) Figure 1 | Disruption of phosphate homeostasis in chronic kidney disease (CKD).

Nat. Rev. Nephrol. doi: /nrneph

Figure 5 A layered approach to the follow-up of patients with acute kidney disease (AKD) Figure 5 | A layered approach to the follow-up of patients with.

Figure 6 Effects of adiponectin on podocyte function

Figure 5 Inter-relationships between sleep apnoea, CKD and brain injury Figure 5 | Inter-relationships between sleep apnoea, CKD and brain injury. In chronic.

Figure 3 Metabolism in homeostatic chondrocytes

Figure 3 Energy metabolism regulation, cardiovascular and bone disease in CKD Figure 3 | Energy metabolism regulation, cardiovascular and bone disease.

Figure 6 Approach to drug management in patients with acute kidney disease (AKD) Figure 6 | Approach to drug management in patients with acute kidney disease.

Figure 4 Expression of coagulation protease receptors in renal cells

جسم الانسان.

Figure 4 Interactions between adipose, the microbiome and kidney

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Figure 2 Physiological changes in the renal system in pregnancy

Figure 2 Proinflammatory mechanisms in CKD

Figure 1 Circadian changes in energy metabolism and immune responses in CKD Figure 1 | Circadian changes in energy metabolism and immune responses in CKD.

Figure 4 Effect of dapagliflozin on HbA1c and body weight

Figure 3 The fat–intestine–kidney axis

Nat. Rev. Nephrol. doi: /nrneph

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Figure 6 The bioavailability of phosphate differs according to the protein source Figure 6 | The bioavailability of phosphate differs according to the.

Figure 7 The efficacy of phosphate-binder therapy

Figure 2 Candidate signalling pathways of irisin in myocytess

Figure 3 Putative actions of glucagon-like peptide 1 (GLP-1)

Figure 1 Immune cell metabolism during homeostasis

Figure 2 Glucose handling by the kidney

Figure 2 The network of chronic diseases and their mutual influences

Figure 1 The sensory and secretory function of the L cell

Figure 1 The burden of chronic kidney disease (CKD)

Figure 3 Societal costs for the care of patients with chronic kidney disease in the UK Figure 3 | Societal costs for the care of patients with chronic.

Figure 2 Metabolic reprogramming of immune cells upon activation

Figure 1 Acute kidney injury and chronic kidney disease

Figure 4 The gut–kidney axis, inflammation and cardiovascular disease in CKD Figure 4 | The gut–kidney axis, inflammation and cardiovascular disease in.

Figure 4 Model of changes in the serum levels

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Figure 2 Roles of mTOR complexes in the kidney

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Figure 5 Potential roles of phosphate and fibroblast growth factor 23 (FGF-23) in the development of cardiovascular disease in patients with chronic kidney.

Figure 1 mTOR complex biology

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Nat. Rev. Nephrol. doi: /nrneph

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Nat. Rev. Nephrol. doi: /nrneph

cardiovascular and renal systems

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Figure 3 Loss of the glycocalyx leads to podocyte and kidney injury

Figure 4 Differential protective effects of hydration

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Figure 5 The nephron-centric model of renal transplant fibrosis based on the injury-related molecular events observed in biopsy samples in the first year.

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Figure 3 Serum phosphate level is associated with

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Figure 3 Regulation of TGF-β1/Smad signalling by microRNAs (miRs) in tissue fibrosis Figure 3 | Regulation of TGF-β1/Smad signalling by microRNAs (miRs)

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Nat. Rev. Nephrol. doi: /nrneph

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Figure 2 Biologics that target CD4+ T helper (TH)-cell subsets

Figure 4 The relationship between the time-dependent changes in the expression of immunoglobulin, mast cell, acute kidney injury (AKI), and fibrillar collagen.

Figure 4 Intracellular distribution and

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Presentation transcript:

Figure 1 Role of the kidney in glucose homeostasis Figure 1 | Role of the kidney in glucose homeostasis. The kidney utilizes glucose as an energy source (renal medullary cells) and produces glucose via gluconeogenesis (renal cortical cells). The net result is that the net arteriovenous balance of glucose across the kidney is zero. Glucose production by the renal cortical cells is inhibited by insulin and stimulated by adrenaline. Glucagon has no effect on renal glucose production. Glutamine is extracted by renal tubular cells and used to generate ammonia (NH3), which has an important role in acid excretion (NH4+). RA, renal artery; RV, renal vein. DeFronzo, R. A. et al. (2016) Renal, metabolic and cardiovascular considerations of SGLT2 inhibition Nat. Rev. Nephrol. doi:10.1038/nrneph.2016.170