Статті в журналах: "Insulin metabolism"

1

Ukkola, O. "Ghrelin and insulin metabolism." European Journal of Clinical Investigation 33, no. 3 (March 2003): 183–85. http://dx.doi.org/10.1046/j.1365-2362.2003.01112.x.

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2

Duckworth, William C., Frederick G. Hamel, and Daniel E. Peavy. "Hepatic metabolism of insulin." American Journal of Medicine 85, no. 5 (November 1988): 71–76. http://dx.doi.org/10.1016/0002-9343(88)90399-3.

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3

Heesom, K. J., M. Harbeck, C. R. Kahn, and R. M. Denton. "Insulin action on metabolism." Diabetologia 40 (September 19, 1997): S3—S9. http://dx.doi.org/10.1007/s001250051388.

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4

Beardsall, Kathryn, Barbro M. S. Diderholm, and David B. Dunger. "Insulin and carbohydrate metabolism." Best Practice & Research Clinical Endocrinology & Metabolism 22, no. 1 (February 2008): 41–55. http://dx.doi.org/10.1016/j.beem.2007.10.001.

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5

Heesom, K. J., M. Harbeck, C. R. Kahn, and R. M. Denton. "Insulin action on metabolism." Diabetologia 40, S3 (March 1997): B3—B9. http://dx.doi.org/10.1007/bf03168179.

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6

Harned, Leighton Kahle, and Edward Chin. "PSUN278 Factitious hypoglycemia, diagnostic delay due to insulin assay failure to detect insulin analogues." Journal of the Endocrine Society 6, Supplement_1 (November 1, 2022): A403. http://dx.doi.org/10.1210/jendso/bvac150.838.

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Abstract Factitious hypoglycemia may be difficult to diagnose clinically. Hypoglycemia due to insulin self-administration is established by the presence of a low c-peptide and elevated plasma insulin levels. Commercial insulin assays often fail to detect insulin analogs and can create confusion among providers investigating causes of hypoglycemia. A 20 year old female with no significant past medical history presented to an Emergency Room (ER) with hypoglycemia. She was treated with a single dose of octreotide 150 mcg, dexamethasone 10 mg PO and started on a D10W drip at 100ml/hr prior to transfer. Laboratory studies on transfer reported plasma glucose 52ng/dL (RR: 70-100), low C-peptide 0.02 (RR: 0.78-5.19), low insulin level <0.087 uIU/mL, normal IGF-I level 122 ng/mL (RR: 85-370). Normal IGF-II level 401 ng/mL (RR: 333-967), and low Pro-insulin level 1.8 pmol/L (RR: 3.6-22 pmol/L). Sulfonylurea Screen was negative. The patient and her mother both denied exogenous insulin use. The patient and her mother both work in healthcare. The patient's boyfriend has type 1 diabetes mellitus and the patient stated she keeps insulin in her purse for him. The patient was admitted for a 72 hour fast and remained normoglycemic. An aliquot of the admission ER insulin blood sample was sent to second laboratory utilizing an assay able to detect analog insulins. The patient's sample previously reporting an undetectable insulin level (<0.087 uIU/mL) now reported an insulin level 8 uIU/mL. Factitious hypoglycemia is a challenging clinical diagnosis. The term factitious implies an attempt to deceive and creates mistrust between the physician and patient. However, hypoglycemia may be the result of medication errors or administered by a second party with the intent to harm. Analog insulins (glargine, aspart, lispro, glulisine, etc) are genetically modified insulins developed to mimic the physiologic pattern of pancreatic beta cell insulin secretion. The amino acid modifications in analog insulins result in structural variations which alters the ability of highly specific commercial automated immunoassays to accurately quantitate these analog insulins. The variation in lab assay detection may cause confusion when interpreting the results. The DiaSorin Liaison XL platform in our hospital utilizes a chemiluminescence immunoassay which does not detect insulin analogs, but detects regular and NPH insulin as they are structurally identical to endogenous human insulin. The second laboratory uses the Siemens Advia Centaur platform, an immunoassay which reacts with insulin analogs "on a nearly equimolar basis with the analogs insulin aspart, insulin glargine, and insulin lispro. Insulin detemir exhibits approximately 50 percent cross-reactivity. Test reactivity with insulin glulisine is negligible (< 3 percent)". Many commercial insulin assays do not detect analog insulins and none qualitatively distinguish between different insulins. Failure to recognize this detection flaw may result in misdiagnosis, patient safety issues and costly unneeded additional studies Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.

7

Kagotho, Elizabeth. "Insulin-Mediated Glucose Metabolism: An Atherogenic Lipid Profile of Fructose Consumption." Endocrinology and Disorders 2, no. 2 (February 27, 2018): 01–02. http://dx.doi.org/10.31579/2640-1045/096.

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Our laboratory has investigated two hypotheses regarding the effects of fructose consumption: 1) The endocrine effects of fructose consumption favor a positive energy balance, and 2) Fructose consumption promotes the development of an atherogenic lipid profile. In previous short- and long-term studies, we demonstrated that consumption of fructose-sweetened beverages with 3 meals results in lower 24-hour plasma concentrations of glucose, insulin, and leptin in humans compared with consumption of glucose-sweetened beverages. We have also tested whether prolonged consumption of high-fructose diets could lead to increased caloric intake or decreased energy expenditure, thereby contributing to weight gain and obesity. Results from a study conducted in rhesus monkeys produced equivocal results. Carefully controlled and adequately powered long-term studies are needed to address these hypotheses. In both short- and long-term studies we demonstrated that consumption of fructose-sweetened beverages substantially increases postprandial triacylglycerol concentrations compared with glucose-sweetened beverages. In the long-term studies, apolipoproteinB concentrations were also increased in subjects consuming fructose, but not those consuming glucose. Data from a short-term study comparing consumption of beverages sweetened with fructose, glucose, high fructose corn syrup (HFCS) and sucrose, suggest that HFCS and sucrose increase postprandial triacylglycerol to an extent comparable to that induced by 100% fructose alone. Increased consumption of fructose-sweetened beverages along with increased prevalence of obesity, metabolic syndrome, and type 2 diabetes underscore the importance of investigating the metabolic consequences fructose consumption in carefully controlled experiments.

8

Kagotho, Elizabeth. "Insulin-Mediated Glucose Metabolism: An Atherogenic Lipid Profile of Fructose Consumption." Endocrinology and Disorders 2, no. 2 (February 15, 2018): 01–02. http://dx.doi.org/10.31579/2640-1045/021.

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9

Kusters, Yvo H. A. M., and Eugene J. Barrett. "Muscle microvasculature's structural and functional specializations facilitate muscle metabolism." American Journal of Physiology-Endocrinology and Metabolism 310, no. 6 (March 15, 2016): E379—E387. http://dx.doi.org/10.1152/ajpendo.00443.2015.

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We review the evolving findings from studies that examine the relationship between the structural and functional properties of skeletal muscle's vasculature and muscle metabolism. Unique aspects of the organization of the muscle microvasculature are highlighted. We discuss the role of vasomotion at the microscopic level and of flowmotion at the tissue level as modulators of perfusion distribution in muscle. We then consider in some detail how insulin and exercise each modulate muscle perfusion at both the microvascular and whole tissue level. The central role of the vascular endothelial cell in modulating both perfusion and transendothelial insulin and nutrient transport is also reviewed. The relationship between muscle metabolic insulin resistance and the vascular action of insulin in muscle continues to indicate an important role for the microvasculature as a target for insulin action and that impairing insulin's microvascular action significantly affects body glucose metabolism.

10

Piloquet, H., V. Ferchaud-Roucher, F. Duengler, Y. Zair, P. Maugere, and M. Krempf. "Insulin effects on acetate metabolism." American Journal of Physiology-Endocrinology and Metabolism 285, no. 3 (September 2003): E561—E565. http://dx.doi.org/10.1152/ajpendo.00042.2003.

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Acetate metabolism was studied in patients with insulin resistance. To evaluate the interaction between glucose and acetate metabolism, we measured acetate and glucose turnover with a hyperinsulinemic euglycemic clamp (hot clamp) in obese and diabetic patients with insulin resistance ( n = 8) and in a control group with normal insulin sensitivity ( n = 6). At baseline, acetate turnover and plasma concentrations were similar between the two groups (group means: 4.3 ± 0.4 μmol · kg-1 · min-1 and 128.2 ± 11.1 μmol/l). Acetate concentrations decreased in both groups with hyperinsulinemia but were significantly lower in the insulin-resistant group (20% vs. 12%, P < 0.05). After the hot clamp treatment, acetate turnover increased for the two groups and was higher in the group with normal insulin sensitivity: 8.1 ± 0.7 vs. 5.5 ± 0.5 μmol · kg-1 · min-1 ( P < 0.001). No change related to insulin action was observed in either group in the percentage of acetate oxidation. This was ≈70% of overall utilization at baseline and during the clamp. No correlation between glucose and acetate utilization was observed. Our results support the hypothesis that, like glucose metabolism, acetate metabolism is sensitive to insulin.

11

TAKAHASHI, Shin-Ichirou. "Hormone and protein metabolism. Insulin and protein metabolism." Journal of the agricultural chemical society of Japan 61, no. 10 (1987): 1300–1304. http://dx.doi.org/10.1271/nogeikagaku1924.61.1300.

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12

Caprio, S., G. Cline, S. Boulware, C. Permanente, G. I. Shulman, R. S. Sherwin, and W. V. Tamborlane. "Effects of puberty and diabetes on metabolism of insulin-sensitive fuels." American Journal of Physiology-Endocrinology and Metabolism 266, no. 6 (June 1, 1994): E885—E891. http://dx.doi.org/10.1152/ajpendo.1994.266.6.e885.

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Insulin's ability to stimulate glucose metabolism is reduced during normal puberty; these changes are exaggerated in adolescents with insulin-dependent diabetes mellitus (IDDM). Because the effects of puberty and IDDM on the other actions of insulin have not been established, we studied leucine kinetics (using [1-13C]leucine) and fat metabolism during euglycemic hyperinsulinemia (20 mU.m2.min-1) for 3 h in eight healthy and nine IDDM (HbA1 14 +/- 2%) adolescents and six healthy young adult controls. IDDM subjects received overnight low-dose insulin infusion to normalize fasting glucose. Basal and steady-state insulin values (approximately 240 pM) during the study were similar in all three groups. Insulin-stimulated glucose metabolism was reduced by 40% in healthy adolescents vs. adults (P < 0.05) and by an additional 40% in poorly controlled IDDM (P < 0.05 vs, normal adolescents). Although basal glucose and lipid oxidation rates (measured by indirect calorimetry) were similar in all three groups, when insulin was infused, glucose oxidation increased and lipid oxidation decreased only in the two nondiabetic groups. Similarly, insulin significantly reduced plasma free fatty acid levels only in the nondiabetics. Basal leucine flux (an index of protein degradation) was similar in healthy controls but was markedly increased in IDDM adolescents. Despite similar increments in plasma insulin during the clamp, leucine flux remained higher in IDDM adolescents than in healthy controls. Basal leucine oxidation rates were also increased in IDDM subjects compared with nondiabetic groups and declined to a lesser extent during insulin infusion. We conclude that insulin resistance of puberty is selective for glucose metabolism, sparing amino acid/protein metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)

13

Hirsch, Irl B., Rattan Juneja, John M. Beals, Caryl J. Antalis, and Eugene E. Wright. "The Evolution of Insulin and How it Informs Therapy and Treatment Choices." Endocrine Reviews 41, no. 5 (May 12, 2020): 733–55. http://dx.doi.org/10.1210/endrev/bnaa015.

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Abstract Insulin has been available for the treatment of diabetes for almost a century, and the variety of insulin choices today represents many years of discovery and innovation. Insulin has gone from poorly defined extracts of animal pancreata to pure and precisely controlled formulations that can be prescribed and administered with high accuracy and predictability of action. Modifications of the insulin formulation and of the insulin molecule itself have made it possible to approximate the natural endogenous insulin response. Insulin and insulin formulations had to be designed to produce either a constant low basal level of insulin or the spikes of insulin released in response to meals. We discuss how the biochemical properties of endogenous insulin were exploited to either shorten or extend the time-action profiles of injectable insulins by varying the pharmacokinetics (time for appearance of insulin in the blood after injection) and pharmacodynamics (time-dependent changes in blood sugar after injection). This has resulted in rapid-acting, short-acting, intermediate-acting, and long-acting insulins, as well as mixtures and concentrated formulations. An understanding of how various insulins and formulations were designed to solve the challenges of insulin replacement will assist clinicians in meeting the needs of their individual patients.

14

Ikeoka, Dimas, and Eva Krusinova. "Insulin resistance and lipid metabolism." Revista da Associação Médica Brasileira 55, no. 3 (2009): 234. http://dx.doi.org/10.1590/s0104-42302009000300003.

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15

Blatniczky, L., L. Kautzky, and F. Péter. "Insulin Metabolism in Hypothalamic Obesity." Experimental and Clinical Endocrinology & Diabetes 96, no. 04 (July 16, 2009): 83–89. http://dx.doi.org/10.1055/s-0029-1210992.

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16

Howard, Barbara V. "Insulin resistance and lipid metabolism." American Journal of Cardiology 84, no. 1 (July 1999): 28–32. http://dx.doi.org/10.1016/s0002-9149(99)00355-0.

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17

Biolo, Gianni, and Robert R. Wolfe. "Insulin action on protein metabolism." Baillière's Clinical Endocrinology and Metabolism 7, no. 4 (October 1993): 989–1005. http://dx.doi.org/10.1016/s0950-351x(05)80242-3.

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18

Frayn, Keith N. "Insulin resistance and lipid metabolism." Current Opinion in Lipidology 4, no. 3 (June 1993): 197–204. http://dx.doi.org/10.1097/00041433-199306000-00004.

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19

Taskinen, Marja-Riitta. "Insulin resistance and lipoprotein metabolism." Current Opinion in Lipidology 6, no. 3 (June 1995): 153–60. http://dx.doi.org/10.1097/00041433-199506000-00007.

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20

Langouche, Lies, and Greet Van den Berghe. "Glucose Metabolism and Insulin Therapy." Critical Care Clinics 22, no. 1 (January 2006): 119–29. http://dx.doi.org/10.1016/j.ccc.2005.09.005.

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21

Davis, T. A., and I. E. Karl. "Resistance of protein and glucose metabolism to insulin in denervated rat muscle." Biochemical Journal 254, no. 3 (September 15, 1988): 667–75. http://dx.doi.org/10.1042/bj2540667.

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Denervated (1-10 days) rat epitrochlearis muscles were isolated, and basal and insulin-stimulated protein and glucose metabolism were studied. Although basal rates of glycolysis and glucose transport were increased in 1-10-day-denervated muscles, basal glycogen-synthesis rates were unaltered and glycogen concentrations were decreased. Basal rates of protein degradation and synthesis were increased in 1-10-day-denervated muscles. The increase in degradation was greater than that in synthesis, resulting in muscle atrophy. Increased rates of proteolysis and glycolysis were accompanied by elevated release rates of leucine, alanine, glutamate, pyruvate and lactate from 3-10-day-denervated muscles. ATP and phosphocreatine were decreased in 3-10-day-denervated muscles. Insulin resistance of glycogen synthesis occurred in 1-10-day denervated muscles. Insulin-stimulated glycolysis and glucose transport were inhibited by day 3 of denervation, and recovered by day 10. Inhibition of insulin-stimulated protein synthesis was observed only in 3-day-denervated muscles, whereas regulation by insulin of net proteolysis was unaffected in 1-10-day-denervated muscles. Thus the results demonstrate enhanced glycolysis, proteolysis and protein synthesis, and decreased energy stores, in denervated muscle. They further suggest a defect in insulin's action on protein synthesis in denervated muscles as well as on glucose metabolism. However, the lack of concurrent changes in all insulin-sensitive pathways and the absence of insulin-resistance for proteolysis suggest multiple and specific cellular defects in insulin's action in denervated muscle.

22

Davis, T. A., S. Klahr, and I. E. Karl. "Glucose metabolism in muscle of sedentary and exercised rats with azotemia." American Journal of Physiology-Renal Physiology 252, no. 1 (January 1, 1987): F138—F145. http://dx.doi.org/10.1152/ajprenal.1987.252.1.f138.

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Insulin resistance has been demonstrated in chronic renal failure patients and may be improved by exercise training, but the mechanisms have not been identified. In this study, the response of glucose uptake, glycogen synthesis, and glucose utilization via glycolysis (glycolytic utilization) to stimulation by insulin and/or acute exercise were determined in isolated muscles from rats with moderate renal insufficiency that were exercise trained or remained sedentary. Moderate renal insufficiency had no effect on the basal rate, insulin sensitivity, or insulin responsiveness of glucose uptake, glycogen synthesis, or glycolytic utilization in muscle. The enhanced insulin responsiveness of both glycogen synthesis and glucose uptake following acute exercise, noted in control animals, was less in rats with moderate renal insufficiency, but the enhanced basal rate and insulin sensitivity after exercise were unaffected by moderate renal insufficiency. Exercise training increased the insulin sensitivity and responsiveness of muscle glucose uptake and glycolytic utilization in rats with moderate renal insufficiency and in controls. The effects of acute exercise and exercise training on insulin responsiveness of glucose uptake were additive in controls but not in animals with moderate renal insufficiency. These findings are compatible with the concept that moderate renal insufficiency is associated with a postreceptor defect in insulin's action in muscle, detectable only following maximal stimulation of glucose transport by insulin and exercise, and partially correctable by exercise training.

23

Bonen, Arend, G. Lynis Dohm, and Luc J. C. van Loon. "Lipid metabolism, exercise and insulin action." Essays in Biochemistry 42 (November 27, 2006): 47–59. http://dx.doi.org/10.1042/bse0420047.

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Skeletal muscle constitutes 40% of body mass and takes up 80% of a glucose load. Therefore, impaired glucose removal from the circulation, such as that which occurs in obesity and type 2 diabetes, is attributable in large part to the insulin resistance in muscle. Recent research has shown that fatty acids, derived from adipose tissue, can interfere with insulin signalling in muscle. Hence, insulin-stimulated GLUT4 translocation to the cell surface is impaired, and therefore, the rate of glucose removal from the circulation into muscle is delayed. The mechanisms provoking lipid-mediated insulin resistance are not completely understood. In sedentary individuals, excess intramyocellular accumulation of triacylglycerols is only modestly associated with insulin resistance. In contrast, endurance athletes, despite accumulating large amounts of intramyocellular triacylglycerols, are highly insulin sensitive. Thus it appears that lipid metabolites, other than triacylglycerols, interfere with insulin signalling. These metabolites, however, are not expected to accumulate in athletic muscles, as endurance training increases the capacity for fatty acid oxidation by muscle. These observations, and others in severely obese individuals and type 2 diabetes patients, suggest that impaired rates of fatty acid oxidation are associated with insulin resistance. In addition, in obesity and type 2 diabetes, the rates of fatty acid transport into muscle are also increased. Thus, excess intracellular lipid metabolite accumulation, which interferes with insulin signalling, can occur as a result of impaired rates of fatty acid oxidation and/or increased rates of fatty acid transport into muscle. Accumulation of excess intramyocellular lipid can be avoided by exercise, which improves the capacity for fatty acid oxidation.

24

Del Prato, S., R. A. DeFronzo, P. Castellino, J. Wahren, and A. Alvestrand. "Regulation of amino acid metabolism by epinephrine." American Journal of Physiology-Endocrinology and Metabolism 258, no. 5 (May 1, 1990): E878—E887. http://dx.doi.org/10.1152/ajpendo.1990.258.5.e878.

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The effect of epinephrine on amino acid (AA) metabolism was examined in 33 healthy volunteers who participated in four studies. Nine subjects participated in study I, which consisted of four parts: euglycemic insulin clamp, insulin plus epinephrine, insulin plus epinephrine plus propranolol, and insulin plus propranolol. In study II six subjects received epinephrine with hepatic-femoral venous catheterization. In study III five individuals received epinephrine with somatostatin plus basal insulin replacement. In study IV quadriceps muscle biopsy was performed in six subjects after epinephrine or insulin infusion. Both epinephrine and insulin caused a generalized decline in all plasma AA except alanine. With combined epinephrine-insulin infusion, the decrease in plasma AA was additive. Propranolol blocked the hypoaminoacidemic effect of epinephrine but failed to alter the AA lowering action of insulin. Epinephrine, while maintaining basal insulinemia, reduced the catechol's hypoaminoacidemic effect by 39%. After epinephrine, splanchnic alanine uptake increased, but plasma alanine remained constant because of a parallel rise in muscle alanine production. Plasma/intracellular concentrations of branched-chain amino acids (BCAA) and all gluconeogenic amino acids, except alanine, decreased after both epinephrine and insulin. In summary, the effect of epinephrine on plasma/intracellular total, gluconeogenic, and BCAA concentrations is similar to insulin.

25

Gargiulo, P., U. Di Mario, O. Zuccarini, F. Troili, C. Tiberti, U. Nicolini, A. Pachi, G. Gerlini, and F. Fallucca. "Treatment of diabetic pregnant women with monocomponent insulins." Acta Endocrinologica 113, no. 3_Suppl (August 1986): S60—S65. http://dx.doi.org/10.1530/acta.0.111s0060.

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Abstract. Very little immunological research has been undertaken in pregnant diabetic women in relation to insulin therapy. We investigated the relations between treatment with insulins of varied immunogenic character and the presence of immune factors such as insulin antibodies, immune complexes and insulin antiinsulin complexes as well as some maternal and neonatal complications of diabetic pregnancy. 128 insulin treated diabetic pregnant women and 121 of their newborns were included in the study. The incidence of insulin antibodies, immune complexes and insulin antiinsulin complexes was lower in patients treated with highly purified insulins than in those treated with conventional insulins. The insulin antibody levels were significantly related to the occurrence of maternal and neonatal morbibity. The presence of insulin antiinsulin complexes in the cord blood of infants of diabetic mothers was related to the presence of these complexes in their mothers. Our results seem to indicate that the use of highly purified insulin could favour the outcome of diabetic pregnancy.

26

Rossetti, L., G. Klein-Robbenhaar, G. Giebisch, D. Smith, and R. DeFronzo. "Effect of insulin on renal potassium metabolism." American Journal of Physiology-Renal Physiology 252, no. 1 (January 1, 1987): F60—F64. http://dx.doi.org/10.1152/ajprenal.1987.252.1.f60.

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The effect of insulin on renal potassium excretion was examined by employing the euglycemic insulin clamp technique in combination with renal clearance measurements. While euglycemia was maintained, insulin was infused at rates of 4.8 (n = 7) and 12 (n = 5) mU X kg-1 X min-1. Steady-state plasma insulin levels of 164 +/- 8 and 370 +/- 15 microU/ml were achieved in the low- and high-dose studies, respectively. Base-line plasma potassium concentration declined progressively by a mean of 0.14 +/- 0.09 (P less than 0.05) and 0.40 +/- 0.05 meq/liter (P less than 0.01) during the low- and high-dose insulin infusion protocols. Urinary potassium excretion did not change significantly from base line with either insulin dose. Because the decline in plasma potassium concentration could have masked a stimulatory effect of insulin on UKV, six rats received a 12-mU X kg-1 X min-1 euglycemic insulin clamp in combination with an exogenous potassium infusion to maintain the plasma potassium concentration constant at the basal level (4.03 +/- 0.03 vs. 4.05 +/- 0.05 meq/l). Under these conditions of normokalemia, insulin augmented UKV 2.4-fold, from 0.20 +/- 0.05 to 0.48 +/- 0.04 meq/l (P less than 0.001).

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Duan, C., T. Noso, S. Moriyama, H. Kawauchi, and T. Hirano. "Eel insulin: isolation, characterization and stimulatory actions on [35S]sulphate and [3H]thymidine uptake in the branchial cartilage of the eel in vitro." Journal of Endocrinology 133, no. 2 (May 1992): 221–30. http://dx.doi.org/10.1677/joe.0.1330221.

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ABSTRACT Our previous studies have shown that mammalian and salmon insulins stimulate sulphate uptake by cultured eel cartilage, suggesting the possible involvement of insulin in the regulation of cartilage matrix synthesis. In the present study, homologous eel insulin was isolated and characterized, and its effects on cartilage matrix synthesis and DNA synthesis were examined in vitro. Insulin was extracted from eel pancreas with acid–ethanol, and subsequently purified by isoelectric precipitation at pH 5·3, gel filtration on Sephadex G-50, and reversed-phase high-performance liquid chromatography. The amino acid composition and complete sequence (50 residues) of eel insulin revealed high homology to teleostean and mammalian insulins. The isolated eel insulin produced a more pronounced and longer lasting hypoglycaemic effect than bovine insulin in the eel. Homologous eel insulin, like bovine insulin-like growth factor (IGF-I) and insulin, stimulated sulphate uptake by cultured eel cartilage in a dose-dependent manner (16–1000 ng/ml). Combination experiments using maximal concentrations of bovine IGF-I (250 ng/ml) and increasing amounts of eel insulin (10–250 ng/ml) showed no additive effects of insulin on sulphate uptake, suggesting that insulin and IGF-I may share a common mechanism(s) of action. Eel insulin and bovine IGF-I also enhanced thymidine incorporation by eel cartilage in a dose-dependent manner (4–1000 ng/ml); eel insulin was equipotent with bovine IGF-I. These results suggest that insulin, like IGF-I, may exert direct growth-promoting actions in branchial cartilage of the eel. Journal of Endocrinology (1992) 133, 221–230

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Danne, Thomas, and Jan Bolinder. "New Insulins and Insulin Therapy." Diabetes Technology & Therapeutics 15, S1 (February 2013): S—40—S—47. http://dx.doi.org/10.1089/dia.2013.1505.

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29

Fryburg, D. A., E. J. Barrett, R. J. Louard, and R. A. Gelfand. "Effect of starvation on human muscle protein metabolism and its response to insulin." American Journal of Physiology-Endocrinology and Metabolism 259, no. 4 (October 1, 1990): E477—E482. http://dx.doi.org/10.1152/ajpendo.1990.259.4.e477.

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Although starvation is known to impair insulin-stimulated glucose disposal, whether it also induces resistance to insulin's antiproteolytic action on muscle is unknown. To assess the effect of fasting on muscle protein turnover in the basal state and in response to insulin, we measured forearm amino acid kinetics, using [3H]phenylalanine (Phe) and [14C]leucine (Leu) infused systemically, in eight healthy subjects after 12 (postabsorptive) and 60 h of fasting. After a 150-min basal period, forearm local insulin concentration was selectively raised by approximately 25 muU/ml for 150 min by intra-arterial insulin infusion (0.02 mU.kg-1. min-1). The 60-h fast increased urine nitrogen loss and whole body Leu flux and oxidation (by 50-75%, all P less than 0.02). Post-absorptively, forearm muscle exhibited a net release of Phe and Leu, which increased two- to threefold after the 60-h fast (P less than 0.05); this effect was mediated exclusively by accelerated local rates of amino acid appearance (Ra), with no reduction in rates of disposal (Rd). Local hyperinsulinemia in the postabsorptive condition caused a twofold increase in forearm glucose uptake (P less than 0.01) and completely suppressed the net forearm output of Phe and Leu (P less than 0.02). After the 60-h fast, forearm glucose disposal was depressed basally and showed no response to insulin; in contrast, insulin totally abolished the accelerated net forearm release of Phe and Leu. The action of insulin to reverse the augmented net release of Phe and Leu was mediated exclusively by approximately 40% suppression of Ra (P less than 0.02) rather than a stimulation of Rd. We conclude that in short-term fasted humans 1) muscle amino acid output accelerates due to increased proteolysis rather than reduced protein synthesis, and 2) despite its catabolic state and a marked impairment in insulin-mediated glucose disposal, muscle remains sensitive to insulin's antiproteolytic action.

30

Gasparyan, E. G., S. A. Nersesyan, Ye A. Volkova, Z. V. Kryuchkova, and L. I. Velikanova. "Minidiab test to assess the function of pancreatic beta-cells in the children of diabetics." Problems of Endocrinology 40, no. 6 (December 15, 1994): 7–10. http://dx.doi.org/10.14341/probl12180.

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The levels of glucose, insulin, and C-peptide in the blood scrum were measured in 38 subjects with normal and impaired glucose tolerance whose parents suffered from insulin-dependent and noninsulin-dependent diabetes mellitus (IDDM and NID- DM, respectively) and in 12 normal subjects without hereditary aggravation for diabetes mellitus in order to specify the pecualiaritics of development of diabetes mellitus of various types. Reliably increased levels of glucose, insulin, and C-peptide on an empty stomach and absence of adequate secretion of insulin and C-peptide in response to stimulation with 5 mg of minidiab, expressed by a later and less manifest release of insulin and C-peptide, were observed in the test group, in contrast to healthy controls. The detected changes augment with the progress of carbohydrate metabolism disorders, being more marked in the subjects whose parents suffered from IDDM. The findings permit a conclusion that function of the insular system is changed during early disorders of carbohydrate metabolism in subjects whose parents suffered from both forms of diabetes mellitus. Minidiab test is recommended to specify the function of the pancreatic insular system.

31

Hanabusa, Tadashi, Chikato Oki, Yoshio Nakano, Kazuhiko Okai, Masahiro Nishi, Hideyuki Sasaki, Tokio Sanke, and Kishio Nanjo. "The renal metabolism of insulin: Urinary insulin excretion in patients with mutant insulin syndrome (insulin Wakayama)." Metabolism 50, no. 8 (August 2001): 863–67. http://dx.doi.org/10.1053/meta.2001.24885.

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32

Demidova, Tatiana Y., and Olga V. Balutina. "Special aspects of concentrated insulins: basic characteristics and research findings." Diabetes mellitus 22, no. 5 (January 17, 2020): 481–90. http://dx.doi.org/10.14341/dm10334.

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The appearance of concentrated insulins in clinical practice determines the need to analyze product priorities in appropriate groups of patients with diabetes. The aim of this article is to summarize the literature on concentrated insulins (i.e. insulin lispro 200 units/mL, insulin degludec 200 units/mL, insulin glargine 300 units/mL) from randomized controlled trials, derive guidance on appropriate and safe use of these agents and demonstrate experience in real clinical practice. Severe hypoglycemia in all studies was generally low (though higher with prandial plus concentrated basal analogue therapy), and statistical improvements in other hypoglycemia categories were observed for concentrated basal insulins versus insulin glargine 100 units/mL. In all analyzed data hypoglycemic effect of insulin glargine 300 units/mL was equitable to insulin glargine 100 units/mL. Other important findings demonstrate more constant and prolonged insulin action with low within-subject/ between-day variability for insulin glargine 300 units/mL versus insulin glargine 100 units/mL, therefore, more physiological treatment might prevent from diabetic microvascular complications. The results of randomized trials are comparable with our clinical practice experience and indicate efficacious and safe glucose-lowering properties without risk of severe hypoglycemia.

33

K Ivaska, Kaisa, Maikki K Heliövaara, Pertti Ebeling, Marco Bucci, Ville Huovinen, H. Kalervo Väänänen, Pirjo Nuutila, and Heikki A Koistinen. "The effects of acute hyperinsulinemia on bone metabolism." Endocrine Connections 4, no. 3 (September 2015): 155–62. http://dx.doi.org/10.1530/ec-15-0022.

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Insulin signaling in bone-forming osteoblasts stimulates bone formation and promotes the release of osteocalcin (OC) in mice. Only a few studies have assessed the direct effect of insulin on bone metabolism in humans. Here, we studied markers of bone metabolism in response to acute hyperinsulinemia in men and women. Thirty-three subjects from three separate cohorts (n=8, n=12 and n=13) participated in a euglycaemic hyperinsulinemic clamp study. Blood samples were collected before and at the end of infusions to determine the markers of bone formation (PINP, total OC, uncarboxylated form of OC (ucOC)) and resorption (CTX, TRAcP5b). During 4 h insulin infusion (40 mU/m2 per min, low insulin), CTX level decreased by 11% (P<0.05). High insulin infusion rate (72 mU/m2 per min) for 4 h resulted in more pronounced decrease (−32%, P<0.01) whereas shorter insulin exposure (40 mU/m2 per min for 2 h) had no effect (P=0.61). Markers of osteoblast activity remained unchanged during 4 h insulin, but the ratio of uncarboxylated-to-total OC decreased in response to insulin (P<0.05 and P<0.01 for low and high insulin for 4 h respectively). During 2 h low insulin infusion, both total OC and ucOC decreased significantly (P<0.01 for both). In conclusion, insulin decreases bone resorption and circulating levels of total OC and ucOC. Insulin has direct effects on bone metabolism in humans and changes in the circulating levels of bone markers can be seen within a few hours after administration of insulin.

34

HIDAKA, T., and T. NOGUCHI. "Regulation of Protein Metabolism by Insulin." Nippon Eiyo Shokuryo Gakkaishi 51, no. 4 (1998): 219–21. http://dx.doi.org/10.4327/jsnfs.51.219.

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35

Sowers, James R., Paul R. Standley, Jeffrey L. Ram, Michael B. Zemel, and Lawrence M. Resnick. "Insulin Resistance, Carbohydrate Metabolism, and Hypertension." American Journal of Hypertension 4, no. 7_Pt_2 (July 1991): 466S—472S. http://dx.doi.org/10.1093/ajh/4.7.466s.

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36

Dagdeviren, Sezin, Anu Shah, Marinna Okawa, Veronika Y. Melnik, Mohsen Sarikhani, Natalie Foot, Sharad Kumar, and Richard T. Lee. "Arrdc4 Regulates Insulin‐Stimulated Glucose Metabolism." FASEB Journal 34, S1 (April 2020): 1. http://dx.doi.org/10.1096/fasebj.2020.34.s1.05395.

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37

JONES, R., and S. OZANNE. "Fetal programming of glucose–insulin metabolism." Molecular and Cellular Endocrinology 297, no. 1-2 (January 15, 2009): 4–9. http://dx.doi.org/10.1016/j.mce.2008.06.020.

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38

Mak, Robert H. K., and Ralph A. De Fronzo. "Glucose and Insulin Metabolism in Uremia." Nephron 61, no. 4 (1992): 377–82. http://dx.doi.org/10.1159/000186953.

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39

Del Prato, S., P. Castellino, D. C. Simonson, and R. A. DeFronzo. "Hyperglucagonemia and insulin-mediated glucose metabolism." Journal of Clinical Investigation 79, no. 2 (February 1, 1987): 547–56. http://dx.doi.org/10.1172/jci112846.

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40

Cheng, Zhiyong, Yolanda Tseng, and Morris F. White. "Insulin signaling meets mitochondria in metabolism." Trends in Endocrinology & Metabolism 21, no. 10 (October 2010): 589–98. http://dx.doi.org/10.1016/j.tem.2010.06.005.

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41

Timmers, Silvie, Patrick Schrauwen, and Johan de Vogel. "Muscular diacylglycerol metabolism and insulin resistance." Physiology & Behavior 94, no. 2 (May 2008): 242–51. http://dx.doi.org/10.1016/j.physbeh.2007.12.002.

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42

OZANNE, S., and C. HALES. "Early programming of glucose–insulin metabolism." Trends in Endocrinology and Metabolism 13, no. 9 (November 1, 2002): 368–73. http://dx.doi.org/10.1016/s1043-2760(02)00666-5.

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43

Petrides, Alexander S., and Ralph A. DeFronzo. "Glucose and insulin metabolism in cirrhosis." Journal of Hepatology 8, no. 1 (January 1989): 107–14. http://dx.doi.org/10.1016/0168-8278(89)90169-4.

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44

Cony, D. B., and M. L. Tuck. "Glucose and Insulin Metabolism in Hypertension." American Journal of Nephrology 16, no. 3 (1996): 223–36. http://dx.doi.org/10.1159/000169002.

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45

Erkelens, D. W. "Insulin resistance and postprandial lipid metabolism." Atherosclerosis 151, no. 1 (July 2000): 79. http://dx.doi.org/10.1016/s0021-9150(00)80357-3.

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46

Gordiunina, S. V. "Insulin resistance in regulation of metabolism." Problems of Endocrinology 58, no. 3 (June 15, 2012): 31–34. http://dx.doi.org/10.14341/probl201258331-34.

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This paper highlights the main causes leading the development of insulin resistance (IR), its mechanisms, and the role it plays in living activity. The analysis of the available literature gives reason to believe that the source of IR is the constant requirement for plastic and high-energy compounds to be mobilized from the body's internal reserves. The mechanisms underlying the development IR involve all organ systems that interact between themselves and thereby govern the origin and evolution of insulin resistance via regulation of the energy generation and consumption processes. This concept is in excellent agreement with the laws of thermodynamics. The vital activity is based on the principle of continuous variations of IR. This inference provides a basis for addressing a number of clinical problems.

47

Howard, Barbara V., Neil Schneiderman, Bonita Falkner, Steven M. Haffner, and Ami Laws. "Insulin, health behaviors, and lipid metabolism." Metabolism 42, no. 9 (September 1993): 25–35. http://dx.doi.org/10.1016/0026-0495(93)90257-o.

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48

Campbell, P. J., M. G. Carlson, and N. Nurjhan. "Fat metabolism in human obesity." American Journal of Physiology-Endocrinology and Metabolism 266, no. 4 (April 1, 1994): E600—E605. http://dx.doi.org/10.1152/ajpendo.1994.266.4.e600.

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Excessive fat turnover and oxidation might cause the insulin resistance of carbohydrate metabolism in obese humans. We studied the response of free fatty acid (FFA) metabolism in lean and obese volunteers to sequential insulin infusions of 4, 8, 25, and 400 mU.m-2.min-1. The insulin dose-response curves for suppression of FFA concentration, FFA turnover ([1-14C]palmitate), and lipolysis ([2H5]glycerol) were shifted to the right in the obese subjects (insulin concentrations that produced a half-maximal response, lean vs. obese: 103 +/- 21 vs. 273 +/- 41, 96 +/- 11 vs. 264 +/- 44, and 101 +/- 23 vs. 266 +/- 44 pM, all P < 0.05), consistent with insulin resistance of FFA metabolism in obesity. After the overnight fast, FFA turnover per fat mass was decreased in obese subjects (37 +/- 4 vs. 20 +/- 3 mumol.kg fat mass-1.min-1, P < 0.01) as the result of suppression of lipolysis by the hyperinsulinemia of obesity and an increased fractional reesterification of FFA before leaving the adipocyte (primary FFA reesterification; 0.14 +/- 0.03 vs. 0.35 +/- 0.06, P < 0.05). Nevertheless, FFA turnover per fat-free mass (FFM) was also greater in the obese volunteers (8.5 +/- 0.7 vs. 11.0 +/- 1.0 mumol.kg FFM-1.min-1, P < 0.05) but only as the result of increased reesterification of intravascular FFA (secondary reesterification; 1.8 +/- 0.5 vs. 4.8 +/- 1.1 mumol.kg FFM-1.min-1, P < 0.01), since FFA oxidation was the same in the two groups throughout the insulin dose-response curve.(ABSTRACT TRUNCATED AT 250 WORDS)

49

Irvine, F., A. V. Wallace, S. R. Sarawak, and M. D. Houslay. "Extracellular calcium modulates insulin's action on enzymes controlling cyclic AMP metabolism in intact hepatocytes." Biochemical Journal 293, no. 1 (July 1, 1993): 249–53. http://dx.doi.org/10.1042/bj2930249.

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Absence of physiological concentrations of extracellular Ca2+ in the Krebs-Henseleit incubation buffer did not affect the ability of 10 nM glucagon (< 5%) to increase hepatocyte intracellular cyclic AMP concentrations, but severely ablated (by approximately 70%) the ability of 10 nM insulin to decrease these elevated concentrations. Cyclic AMP metabolism is determined by production by adenylate cyclase and degradation by cyclic AMP phosphodiesterase (PDE). In the absence of added extracellular Ca2+ (2.5 mM), insulin's ability to activate PDE activity was selectively compromised, showing a failure of insulin to activate two of the three insulin-stimulated activities, namely the ‘dense-vesicle’ and peripheral plasma-membrane (PPM) PDEs. In the absence of added Ca2+, insulin's ability to inhibit adenylate cyclase activity in intact hepatocytes was decreased dramatically. Vasopressin and adrenaline (+ propranolol) failed to elicit the activation of either the ‘dense-vesicle’ or the PPM-PDEs. The presence of physiological concentrations of extracellular Ca2+ in the incubation medium is shown to be important for the appropriate generation of insulin's actions on cyclic AMP metabolism.

50

Borelli, María I., Flavio Francini, and Juan José Gagliardino. "Autocrine regulation of glucose metabolism in pancreatic islets." American Journal of Physiology-Endocrinology and Metabolism 286, no. 1 (January 2004): E111—E115. http://dx.doi.org/10.1152/ajpendo.00161.2003.

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We evaluated the possible autocrine modulatory effect of insulin on glucose metabolism and glucose-induced insulin secretion in islets isolated from normal hamsters. We measured 14CO2 and 3H2O production from d-[U-14C]glucose and d-[5-3H]glucose, respectively, in islets incubated with 0.6, 3.3, 8.3, and 16.7 mM glucose alone or with 5 or 15 mU/ml insulin, anti-insulin guinea pig serum (1:500), 25 μM nifedipine, or 150 nM wortmannin. Insulin release was measured (radioimmunoassay) in islets incubated with 3.3 or 16.7 mM glucose with or without 75, 150, and 300 nM wortmannin. Insulin significantly enhanced 14CO2 and 3H2O production with 3.3 mM glucose but not with 0.6, 8.3, or 16.7 mM glucose. Addition of anti-insulin serum to the medium with 8.3 and 16.7 mM glucose decreased 14CO2 and 3H2O production significantly. A similar decrease was obtained in islets incubated with 8.3 and 16.7 mM glucose and wortmannin or nifedipine. This latter effect was reversed by adding 15 mU/ml insulin to the medium. Glucose metabolism was almost abolished when islets were incubated in a Ca2+-deprived medium, but this effect was not reversed by insulin. No changes were found in 14CO2 and 3H2O production by islets incubated with 3.3 mM glucose and anti-insulin serum, wortmannin, or nifedipine in the media. Addition of wortmannin significantly decreased insulin release induced by 16.7 mM glucose in a dose-dependent manner. Our results suggest that insulin exerts a physiological autocrine stimulatory effect on glucose metabolism in intact islets as well as on glucose-induced insulin release. Such an effect, however, depends on the glucose concentration in the incubation medium.

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