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A student with a ‘hangover’
Published in Tim French, Terry Wardle, The Problem-Based Learning Workbook, 2022
DKA results from either insulin deficiency or an excess of stress hormones with anti-insulin activity. Insulin deficiency results in increased gluconeogenesis in the liver, decreased peripheral glucose uptake and increased lipolysis in adipose tissue. The net result is severe dehydration from a rapid glucose driven osmotic diuresis, and metabolic acidosis from the eventual accumulation of keto acids produced by fatty acid metabolism.
Selected topics
Published in Henry J. Woodford, Essential Geriatrics, 2022
Hyperosmolar hyperglycaemic syndrome (HHS) is a combination of severe hyperglycaemia (30 mmol/L or over), high serum osmolality (320 mOsmol/kg or over) and dehydration (typically 10 to 20% of body weight, or around 10 L water deficit). Patients often present with hypoactive delirium, tachycardia and hypotension. The onset is slow, over several days, which results in an extreme metabolic imbalance. Patients are not, or only mildly, acidotic (serum pH > 7.30, bicarbonate >15). They may be mildly ketotic. The dehydration is caused by osmotic diuresis. HHS is often provoked by inadequate insulin therapy or infection (i.e. pneumonia) plus dehydration. It can be the first presentation of type 2 diabetes. Medications, e.g. oral steroids or atypical antipsychotics, can sometimes precipitate it. Mortality is around 15–20%.140
The endocrine system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
The loss of glucose via the urine promotes an osmotic diuresis, causing dehydration and thirst. In the liver, excess free fatty acids are converted into ketone bodies, which, in the absence of available glucose, are metabolized for cellular energy. The ketone bodies produce a metabolic acidosis (ketoacidosis). If untreated this metabolic disturbances produces hyperosmolarity, hypovolaemia, acidosis, and electrolyte imbalance, which have serious effects on the functions of neurons and result in diabetic ketoacidosis.
Effect of S-allylcysteine against diabetic nephropathy via inhibition of MEK1/2-ERK1/2-RSK2 signalling pathway in streptozotocin-nicotinamide-induced diabetic rats
Published in Archives of Physiology and Biochemistry, 2023
V. V. Sathibabu Uddandrao, Brahmanaidu Parim, Ravindarnaik Ramavat, Suresh Pothani, S. Vadivukkarasi, Ponmurugan P, Chandrasekaran P, Saravanan Ganapathy
The proposed investigation uncovered that in the DN control group of rats revealed the polyurea, polydipsia, polyphagia and increased faecal production considerably as indications of DM and its associated complications (Wang-Fischer and Garyantes 2018). This can be explained by reality that the renal tubules are unequipped for taking up the entirety of the glucose separated in the glomeruli. The renal discharge of glucose requires drainage of water and delivers an osmotic diuresis. It can cause lack of hydration, following in obscured vision and dry skin, which is because of swaying in the measure of water and glucose in the focal points of the eye during parchedness. Loss of water causes an increase in the serum extremity that supports the thirst place in the hypothalamus (Leib et al. 2016). The adaptive raise in food intake induced by diminution of energy stores in these animals involves the synchronised regulation of various pathways within the hypothalamic arcuate nucleus (ARC), a region of the brain that acts as an integration centre for peripheral signals of energy condition. Under basal circumstances, leptin and insulin are thought to hold back ARC neurons that coexpress neuropeptide Y and agouti generelated protein, peptides that potentially excite food intake (Schwartz et al. 2003). Additionally, it was likewise discovered that SAC fundamentally diminished the diabetic attributes, for example, polyphagia, polydipsia and polyurea which may be because of the counter diabetic capability of the SAC (Saravanan et al. 2009).
The therapeutic prospect of zinc oxide nanoparticles in experimentally induced diabetic nephropathy
Published in Tissue Barriers, 2023
Samia A. Abd El-Baset, Nehad F. Mazen, Rehab S. Abdul-Maksoud, Asmaa A. A. Kattaia
Aquaporins (AQPs), transmembrane channels, selectively transport water and some solutes across the cell. AQPs include 13 members (AQP0–AQP12), eight of them (AQP1–AQP7 and AQP11) are distributed in different parts of the kidney47, 48. AQP11 is mainly expressed in the proximal tubules, associated with the endoplasmic reticulum, and controlled by glucose. AQP11 plays an important role in the homeostasis of endoplasmic reticulum and in maintaining the osmolality of cytosol and vesicles. A recessive mutation in mouse AQP11 (Cysteine 227 to Serine 227) resulted in damage of the proximal tubules and renal failure in mutant animals.11 In the present work, there was statistically significant reduction in AQP11 immune histochemical expression in the diabetic group when compared to the controls. AQP11 inadequacy disposes to diabetic kidney disease and hyperglycemia-stimulated renal dysfunction.49 Previously, diabetic polyuria was believed to result from osmotic diuresis due to hyperglycemia. Later, it was found that polyuria is caused by AQPs disorders.50
Extending the ambit of SGLT2 inhibitors beyond diabetes: a review of clinical and preclinical studies on non-diabetic kidney disease
Published in Expert Review of Clinical Pharmacology, 2021
Saurabh Nayak, Vinay Rathore, Joyita Bharati, Kamal Kant Sahu
Four decades ago, a nonselective SGLT inhibitor, phloridzin, was reported to exert a uricosuric effect [119]. Earlier findings suggested the importance of tubular glucose (osmotic diuresis) for uric acid-lowering action. However, a recent preclinical study confirmed the role of GLUT9 and URAT1 transporter in the mediation of the uricosuric potential of SGLT2i [120,121]. Glucosuria also mediates the uricosuric effect through the alteration of uric acid reabsorption. Numerous clinical data confirm the lowering of serum uric acid levels with the administration of SGLT2i within days [122]. Fractional excretion of uric acid is affected by euglycemia and CKD (eGFR< 60 ml/min) stage. The uricosuric effect of SGLT2i among non-diabetics has not been tested in any study involving humans. In non-diabetic mice, URAT1 inhibition is required for the acute uricosuric effect of canagliflozin [120]. In a post hoc analysis, canagliflozin reduced gout flare among T2DM [123]. To date, several clinical studies have provided evidence that uric acid-lowering therapy may help to prevent and delay the decline of renal function in patients with CKD [124]. Also, uric acid-lowering therapy is indicated for cardiovascular protection in CKD patients. The uricosuric effect would be complementary to the overall renoprotection offered by SGLT2i.