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Interaction of Taste and Ingestion
Published in Robert H. Cagan, Neural Mechanisms in Taste, 2020
When blood glucose is elevated, insulin levels also rise through endogenous release. Insulin itself has been shown to depress feeding behavior when administered in physiological doses which fall short of causing pronounced hypoglycemia.193–196 Therefore, Giza and Scott also studied the effects of hyperinsulinemia on taste responses.197 An intravenous injection of 0.5 U/kg regular insulin caused a sharp rise in plasma insulin, with a return to baseline over 90 min. This was accompanied by a modest decline in blood glucose levels that was insufficient to initiate hypoglycemic feeding.198,199 Concomitantly, glucose-evoked activity in the NTS was suppressed by as much as 33% and returned to preinjection levels within 20 min. Responses to fructose were similarly affected, but activity evoked by NaCl, HC1, and quinine was unaltered.
Energy balance and its regulation
Published in Geoffrey P. Webb, Nutrition, 2019
Normal mice lie between these two extremes but inducing obesity by dietary means reduces leptin sensitivity. Diabetes offers a clear precedent for diet and lifestyle causing increased production and declining sensitivity to a hormone. In the common type-2 diabetes, there is no primary failure of the pancreas to produce insulin. A lifestyle of inactivity, high-fat diet and excessive weight gain triggers a progressive decrease in the sensitivity to insulin in response to high insulin secretion. In the more severe but less common type-1 diabetes there is β-cell destruction and an almost complete failure of insulin secretion; this condition requires regular insulin injections for survival. Zhang and Scarpace (2006) review results from several studies which suggest that high circulating leptin levels lead directly to reduced leptin sensitivity by reducing the number of leptin receptors in the hypothalamus. Increased leptin production caused by increased adipose tissue mass directly contributes to leptin resistance and thus promotes further weight gain leading to a vicious cycle of:
Insulin Therapy for Diabetes: Current Scenario and Future Perspectives
Published in Debarshi Kar Mahapatra, Sanjay Kumar Bharti, Medicinal Chemistry with Pharmaceutical Product Development, 2019
Yogesh A. Kulkarni, R. S. Gaud, Mayuresh S. Garud
Human insulin was the first insulin prepared by using recombinant DNA technology [5]. It has identical peptide sequence and tertiary structure to that of endogenous insulin. It is being used as a bolus insulin and is referred as short acting human insulin. It mimics the response of endogenous insulin and corrects the intermeal and premealhyperglycemia. When used in low concentration, the regular insulin solution gets rapidly absorbed in the blood stream after subcutaneous administration. But in high concentration solutions, it has the tendency to get self-aggregate into quaternary and hexamers in the presence of zinc ions [6, 7]. This causes delay in its absorption as it needs to dissociate into diamer and monomer first.
The role of Recent Pharmacotherapeutic Options on the Management of Treatment Resistant Type 2 Diabetes
Published in Expert Opinion on Pharmacotherapy, 2022
Jeffrey M. Kroopnick, Stephen N. Davis
Pre-mixed insulin typically includes an intermediate-acting insulin, such as NPH, and either short-acting regular insulin or a rapid-acting insulin. Given its individual components, premixed insulin is typically dosed twice daily, with breakfast and dinner. These insulins do not provide greater glycemic control compared to a basal-bolus regimen. In a 3-year open-label, multicenter trial consisting of approximately 700 participants aged 18 or older with at least a 12-month history of insulin-naive type 2 diabetes with HbA1c 7–10% despite taking maximally tolerated metformin and a sulfonylurea for at least 4 months, subjects were randomly assigned to pre-mixed biphasic insulin aspart (NovoMix 30), prandial insulin aspart three times daily, or once daily detemir (twice daily if needed). There was no difference in median A1c among the three groups (7.1%, 6.8%, and 6.9%, respectively). However, more patients in the basal (43.2%, p = 0.03) and prandial groups (44.7%, p = 0.006) achieved HbA1c less than or equal to 6.5% compared to the biphasic aspart group [37].
Improving the treatment of patients with diabetes using insulin analogues: current findings and future directions
Published in Expert Opinion on Drug Safety, 2021
Eveline Lefever, Joke Vliebergh, Chantal Mathieu
The major mismatch in action profile is seen with the use of the human insulins. Rapid-acting regular insulin has the same structure as human insulin and consists of six monomers of insulin, organized in a hexamer. To exert its function, an insulin hexamer has to dissociate into monomers to interact with the insulin receptors on target tissues. Injecting regular insulin into the bloodstream leads to immediate dissociation into monomers and consequently an almost immediate onset of action. Nevertheless, regular insulin is normally injected into subcutaneous tissue and has to dissociate into monomers before absorption into the bloodstream is possible. This leads to a delayed onset of action (15–30 minutes) and a variable action profile, which causes postprandial hyperglycemia and delayed hypoglycemia. To overcome the delayed onset of action, people are advised to inject insulin 15–30 min before mealtime, which is inconvenient in daily life [5,13].
Hypoglycemia and lactic acidosis outperform King’s College criteria for predicting death or transplant in acetaminophen toxic patients
Published in Clinical Toxicology, 2018
Michael Levine, Samuel J. Stellpflug, Anthony F. Pizon, David A. Peak, Janna Villano, Timothy Wiegand, Christian Dib, Stephen H. Thomas
Hepatic injury was defined as an aspartate transaminase (AST) or an alanine transaminase (ALT) exceeding 1000 IU/L at any point during the index hospitalization. Length of the stay was defined in calendar days, not 24 h periods. This study utilized a composite endpoint of liver transplant or death. The King’s College criteria include a creatinine of 3.4 mg/dL as one of the endpoints. Patients who were started on continuous renal replacement therapy (CRRT) or hemodialysis prior to reach a creatinine of 3.4 mg/dL were considered to have met these criteria, as we assumed that creatinine would likely rise to that level without intervention in that context of acute renal insufficiency. The King’s College “endpoint” for coagulopathy and acidosis were defined as a prothrombin time (PT) > 100 s and a pH of <7.30, respectively. An “elevated” PT or lactic acid was defined as any laboratory value above the hospital’s reference range. Metabolic acidosis was defined as a pH ≤7.30. Hypoglycemia was defined as a venous or capillary glucose <50 mg/dL. In cases of exogenous insulin administration, the hypoglycemic episode must not have been within 3 h of the administration of regular insulin to be considered. For purposes of calculations, any glucose reading of “low” or “less than 5 mg/dL” was interpreted as 0. Similarly, any laboratory parameter that was recorded as “greater than XX” was interpreted as that result (e.g., an AST >60,000 IU/L was interpreted as 60,000 for purposes of calculations).