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Journal articles on the topic 'Insulin resistance diabete'

Author: Grafiati

Published: 9 June 2023

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1

Feng, Jiayue, and Xiaoping Chen. "A9353 Assessing hip index as a marker for insulin resistance in the general Chinese population without diabete." Journal of Hypertension 36 (October 2018): e153. http://dx.doi.org/10.1097/01.hjh.0000548621.12493.c8.

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2

Druet, C., V. Baltaks??, M. Dabbas, G. Sebag, S. Dorgeret, R. Hankard, D. Chevenne, M. Polak, and C. Levy-Marchal. "O0057 OBESE CHILDREN WITH HIGH RISK OF DIABETE HAVE A REAL INSULIN RESISTANCE (IR) BUT NO DETERIORATION OF GLUCOSE TOLERANCE." Journal of Pediatric Gastroenterology and Nutrition 39, Supplement 1 (June 2004): S29. http://dx.doi.org/10.1097/00005176-200406001-00059.

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3

Adiga, Usha, Kathyayani P, and Nandith P.B. "Association of Insulin Based Insulin Resistance with Liver Biomarkers in Type 2 Diabetes mellitus." Journal of Pure and Applied Microbiology 13, no. 2 (June 30, 2019): 1199–205. http://dx.doi.org/10.22207/jpam.13.2.60.

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4

Maqbool, Mudasir. "Role of Insulin Resistance in Gestational Diabetes Mellitus: A Literature Review." Chettinad Health City Medical Journal 11, no. 02 (June 30, 2022): 69–74. http://dx.doi.org/10.24321/2278.2044.202218.

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Several physiologic, hormonal, and molecular processes contribute to the emergence of hyperglycaemia during pregnancy. Increased insulin resistance is seen during the course of a healthy pregnancy. During the early stages of normal pregnancies, the pancreatic β-cells secrete more insulin, which slows the rise in plasma glucose levels. This regulation explains the abnormally modest increases in plasma glucose levels brought on by elevated insulin resistance. The aim of this review was to evaluate the role of insulin resistance in gestational diabetes mellitus (GDM). The authors extensively searched various electronic databases like PubMed, Scopus, and Google Scholar for the collection of material regarding the role of insulin resistance in GDM. It was seen that hyperglycaemia results from the combination of the pregnancy’s increased insulin tolerance and pancreatic beta-cell insufficiency. Scientific studies have revealed that individuals who present with GDM are more likely to acquire chronic insulin resistance because of the superimposition of lower insulin production by the cells in that condition (GDM). Due to their significance in the development of postpartum diabetes mellitus, inflammation markers in GDM have been widely researched. Inflammation during GDM induces adaptive reactions in the placenta, which can have a substantial effect on the programming of foetal development.

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5

Premkumar, Daivasikamani. "The Role of Obesity in Producing Type 2 Diabetes by Insulin Resistance." Diabetes & Obesity International Journal 5, no. 2 (2020): 1–9. http://dx.doi.org/10.23880/doij-16000227.

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Obesity is a common condition due wrong eating habits and less physical activity. But it can produce serious illness like type 2 diabetes. In Malaysia 18 years and above 33.3% (5.4 million) are pre-obese and 27.2% (4.4 million) are obese. 7.2% are known to have diabetes and 8.0% are previously undiagnosed with diabetes. There is a strong relationship between obesity and diabetes mellitus. We must understand the mechanism by which obesity causes diabetes through and insulin resistance. When the fat distribution is more peripheral have more insulin sensitivity than whose fat distribution is more in the waist. The insulin resistance is caused by variety of substances like non-esterified fatty acids, glycerol, hormones, cytokines, proinflammatory markers which leads to the development of insulin resistance. The development of diabetes is a combination of the failure of β-islet cells of the pancreas and insulin resistance. There is a rising incidence of type 1 and type 2 diabetes due to obesity and weight gain. The obesity is more common in females. Obesity increases with age. Similarly, the incidence of diabetes also increases with and in male sex. Out of 219 persons 77 had normal BMI (less than 25), 83 were overweight (BMI 25 to 30) and 59 were obese (more than 30). The incidence of overweight (37.8%) and obese (26%). People who are overweight (BMI 25- 30) below 40 years are 8, between 40-60 years are 36 and above 60 years are 39. The people who are obese in the 40 years age group 6, 40-60 years 23 and above 60 years 30. Incidence of overweight and obese is more in the females 72.7% and males 58.4%. Incidence of overweight among female is 42% and obese are 30%. Comparatively among male 34.4% are overweight and 24% are obese.

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6

McClain, D. A., and E. D. Crook. "Hexosamines and insulin resistance." Diabetes 45, no. 8 (August 1, 1996): 1003–9. http://dx.doi.org/10.2337/diabetes.45.8.1003.

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7

Coghlan, M. P., and D. M. Smith. "Introduction to the Kinases in Diabetes Biochemical Society focused meeting: are protein kinases good targets for antidiabetic drugs?" Biochemical Society Transactions 33, no. 2 (April 1, 2005): 339–42. http://dx.doi.org/10.1042/bst0330339.

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Insulin regulates whole-body glucose homoeostasis by modulating the activities of protein kinases in its target tissues: muscle, liver and fat. Defects in insulin's ability to modulate protein kinase activity lead to ‘insulin resistance’ or impaired insulin action. Insulin resistance in combination with defective insulin secretion from the pancreas results in the elevated blood glucose levels that are characteristic of diabetes mellitus. Pharmacological agents that selectively modulate protein kinase activities in insulin-resistant tissues may act either as insulin-sensitizing or insulin-mimetic drugs. Consistent with this, small molecule modulators of a number of protein kinases have demonstrated efficacy in animal models of insulin resistance and diabetes. Moreover, emerging data in humans suggest that marketed anti-diabetic agents may also act in part through modulating protein kinase activities. This meeting was convened to consider the potential to treat insulin resistance and Type II diabetes by modulating protein kinase activity.

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8

Kraegen, E. W., P. W. Clark, A. B. Jenkins, E. A. Daley, D. J. Chisholm, and L. H. Storlien. "Development of muscle insulin resistance after liver insulin resistance in high-fat-fed rats." Diabetes 40, no. 11 (November 1, 1991): 1397–403. http://dx.doi.org/10.2337/diabetes.40.11.1397.

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9

Mykkanen, L., D. J. Zaccaro, L. E. Wagenknecht, D. C. Robbins, M. Gabriel, and S. M. Haffner. "Microalbuminuria is associated with insulin resistance in nondiabetic subjects: the insulin resistance atherosclerosis study." Diabetes 47, no. 5 (May 1, 1998): 793–800. http://dx.doi.org/10.2337/diabetes.47.5.793.

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10

Gokcen, Pinar, and Kamil zdil. "A Risk Factor In The Development of Hepatocellular Carcinoma: Insulin Analogues Running Title: Insulin Analogues as a Risk Factor for Liver Cancer." Annals of Medical Research 29, no. 11 (2022): 1. http://dx.doi.org/10.5455/annalsmedres.2022.02.051.

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Aim: The most important mechanisms in the pathogenesis of the relationship between diabetes mellitus and cancer; hyperglycemia, insulin resistance and the inflammation resulting from the activation of insulin receptors. Apart from insulin resistance, hyperinsulinemia may also occur with the use of exogenous insulin. We aimed to investigate the effect of diabetes mellitus and insulin use as a risk factor for hepatocellular carcinoma development in a large patient population with chronic hepatitis B cirrhosis. Materials and Methods: 493 chronic hepatitis B-associated cirrhotic patients were included in the study. The patients were evaluated at 3-6month intervals during follow-up for hepatocellular carcinoma screening. Demographic and laboratory variables, presence of diabetes mellitus, insülin usage, and hepatocellular carcinoma occurrence were recorded. Results: The mean age of patients was 53.5±13.9 years, and 66.2% were male. 18.7% of the patients had a diagnosis of diabetes mellitus and 12% of the patients had insulin use. 68 patients (13.8%) were decompensated cirrhotic. The mean follow-up period was 50.6±33.6 months, during which 43 patients (8.7%) developed hepatocellular carcinoma. In the multivariable analysis, older age, male gender, presence of decompensation, use of exogenous insulin were associated with HCC occurrence (all p<0.05) Conclusion: Diabetes mellitus and insulin resistance have been associated with many cancers due to insulins mitogenic effects. We showed that insulin use is a risk factor for hepatocellular carcinoma development in our chronic hepatitis B-associated cirrhotic patients. Further studies including antidiabetic treatment subgroups are needed.

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11

Goran, M. I., and B. A. Gower. "Longitudinal Study on Pubertal Insulin Resistance." Diabetes 50, no. 11 (November 1, 2001): 2444–50. http://dx.doi.org/10.2337/diabetes.50.11.2444.

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12

Muller-Wieland, D., R. Taub, D. S. Tewari, K. M. Kriauciunas, S. Sethu, K. Reddy, and C. R. Kahn. "Insulin-receptor gene and its expression in patients with insulin resistance." Diabetes 38, no. 1 (January 1, 1989): 31–38. http://dx.doi.org/10.2337/diabetes.38.1.31.

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13

Haffner, S. M., R. D'Agostino, M. F. Saad, M. Rewers, L. Mykkanen, J. Selby, G. Howard, et al. "Increased insulin resistance and insulin secretion in nondiabetic African-Americans and Hispanics compared with non-Hispanic whites. The Insulin Resistance Atherosclerosis Study." Diabetes 45, no. 6 (June 1, 1996): 742–48. http://dx.doi.org/10.2337/diabetes.45.6.742.

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14

Chaoji, Sunanda Ashutosh. "Insulin Resistance." Vidarbha Journal of Internal Medicine 33 (April 6, 2023): 27–31. http://dx.doi.org/10.25259/vjim_41_2022.

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The twin epidemic of ‘Diabesity’-diabetes and obesity, all over the world, both in developed and developing countries, has brought the issue of insulin resistance (IR) into new focus of research. Apart from Type 2 diabetes mellitus (DM), IR is implicated in many other clinical syndromes because of its varied metabolic and mitogenic actions. IR has been found to play important pivotal role in pathophysiology of diabesity. IR is defined as when a normal or higher insulin level fails to produce expected biological response; one predominantly affecting insulin mediated glucose disposal 20–30% reduction in the number of insulin receptors on the target cells is observed in majority of Type 2 DM patients but 1/3 of the patients may not manifest loss of number of receptors; therefore, defective post-receptor signalling is considered as the main cause of IR. Main sites of IR are liver, adipose tissue and skeletal muscles. Apart from Type 2 DM, many other clinical and genetic syndromes are associated with IR.

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15

Wagenknecht, L. E., C. D. Langefeld, A. L. Scherzinger, J. M. Norris, S. M. Haffner, M. F. Saad, and R. N. Bergman. "Insulin Sensitivity, Insulin Secretion, and Abdominal Fat: The Insulin Resistance Atherosclerosis Study (IRAS) Family Study." Diabetes 52, no. 10 (September 26, 2003): 2490–96. http://dx.doi.org/10.2337/diabetes.52.10.2490.

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16

Nolé, Tsabang. "Conditions for Better uses of Some Cameroonian Plants Potentially Anti-Diabetic and Reversing Insulin Resistance." Diabetes & Obesity International Journal 5, no. 1 (2020): 1–15. http://dx.doi.org/10.23880/doij-16000222.

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Background: Hyperglycemia-induced oxidative and inflammatory harm are the major causes of chronic and fatal complications of diabetes. In many developing countries the products of socio-cultural medicine are more used by low income populations to fight against diseases particularly diabetes. The economic crises, the slump of agricultural product’s prizes and the significant increase of the population, are at the origin of the strong dependence on African traditional medicine. Objective: The objectives were to identify factors that influenced the better uses of potential bioactive plants published by Cameroonians, particularly used for diabetes management in order to select those that can improve insulin sensitivity and can be principally used to avoid diabetic complications. Methods: To achieve this objective, the review was carried out in online databases including Google, Google Scholar and Pubmed, between 2018 and 2019. For the ethnopharmacological standardization of recipes, we proposed in this work the doses calculated by deduction from the doses used to treat in vivo alloxan or streptozotocin induced diabetic rats. The presence of one or several antihyperglycemic compounds in recorded plants and the hypoglycemic effects of their extract reinforced the herbal use of these species. Results: All the admitted plants exhibited antidiabetic properties. Twenty-eight point fifty-seven percent (28, 57%) of them were confirmed antihyperglycemic and improved insulin sensitivity. Permanent stress is the important factor influencing the better management of diabetes by these plants. 1.5. Conclusion: The results of this study can be the scientific basis for antidiabetic drugs discovery that can prevent insulin resistant and consequently complications of diabetes type 2.

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17

Wang, J., S. Obici, K. Morgan, N. Barzilai, Z. Feng, and L. Rossetti. "Overfeeding Rapidly Induces Leptin and Insulin Resistance." Diabetes 50, no. 12 (December 1, 2001): 2786–91. http://dx.doi.org/10.2337/diabetes.50.12.2786.

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18

Kobayashi, M., T. Sasaoka, Y. Takata, A. Hisatomi, and Y. Shigeta. "Insulin resistance by uncleaved insulin proreceptor. Emergence of binding site by trypsin." Diabetes 37, no. 5 (May 1, 1988): 653–56. http://dx.doi.org/10.2337/diabetes.37.5.653.

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19

Krook, A., S. Kumar, I. Laing, A. J. Boulton, J. A. Wass, and S. O'Rahilly. "Molecular scanning of the insulin receptor gene in syndromes of insulin resistance." Diabetes 43, no. 3 (March 1, 1994): 357–68. http://dx.doi.org/10.2337/diabetes.43.3.357.

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20

Ogihara, T., T. Asano, K. Ando, Y. Chiba, N. Sekine, H. Sakoda, M. Anai, et al. "Insulin Resistance With Enhanced Insulin Signaling in High-Salt Diet-Fed Rats." Diabetes 50, no. 3 (March 1, 2001): 573–83. http://dx.doi.org/10.2337/diabetes.50.3.573.

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21

Opalenyk, S. M., and S. V. Patskun. "Leptin Resistance as a Risk Marker of Type 2 Diabetes Mellitus in Obese Patients." Ukraïnsʹkij žurnal medicini, bìologìï ta sportu 7, no. 5 (November 21, 2022): 130–33. http://dx.doi.org/10.26693/jmbs07.05.130.

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The purpose of the study was to investigate the influence of leptin resistance on the formation of the risk of type 2 diabetes mellitus in obese patients. Materials and methods. We monitored 50 obese patients who consulted an endocrinologist and a gastroenterologist-nutritionist during 2021-2022. The diagnosis of obesity was made on the basis of bioimpedance examination, as well as by calculating the body mass index. Results and discussion. The article describes and analyzes the level of leptin and leptin resistance as a marker of the risk of type 2 diabetes mellitus in obese patients. To establish the diagnosis of obesity, all patients underwent a bioimpedance examination, and the body mass index was also calculated. Obesity was diagnosed when the body fat content of women was more than 40%, men – more than 28%, and body mass index – more than 30 kg/m2. To identify the syndrome of insulin resistance, the index of insulin resistance was calculated according to the formula: HOMA-IR = fasting insulin (μIU/ml) x fasting glucose (mmol/l) / 22.5. Values exceeding 2.0 were considered insulin resistance. Leptin resistance was diagnosed by determining the presence of the leptin receptor gene and leptin level in blood serum. Leptin resistance was considered to be values of leptin indicators for men more than 5.6 ng/ml, for women – more than 11.1 ng/ml. The level of leptin in blood serum in the group of healthy individuals was within the range of 6.36 ± 2.09 ng/ml in women and 2.96 ± 1.84 ng/ml in men. On the other hand, in obese patients, the serum leptin concentration was 51.49 ± 8.33 ng/ml and 29.71 ± 6.93 ng/ml, respectively. Also, according to the results of the study, a significantly higher level of insulin resistance was observed in all obese patients compared to the control group. These values were at the level of 6.64 ± 2.81 and 7.11 ± 3.52, respectively. Analyzing the results of the study, a reliable relationship between the level of leptin and the severity of obesity was found in all patients. A clear relationship between leptin level and the degree of insulin resistance was also determined. A correlation between the level of leptin and HOMA-IR (r=0.70333; p=0.052) was established, as well as a correlation between fat content, body mass index, leptin level and HOMA-IR (r=0.86187, р=0.0086; r=0.93595, р=0.009; r=0.78098, р=0.007). The detected changes indicate a possible role of leptin and leptin resistance in the pathogenesis of type 2 diabetes mellitus and indicate that the level of leptin can be used as a predictor of the risk of developing type 2 diabetes mellitus in obese patients. Conclusion. An increase in leptin level in blood serum is observed in obese patients. The level of leptin affects the degree of insulin resistance and can be an additional marker of the risk of type 2 diabetes mellitus in obese patients

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22

McClain, D. A., R. R. Henry, A. Ullrich, and J. M. Olefsky. "Restriction-fragment-length polymorphism in insulin-receptor gene and insulin resistance in NIDDM." Diabetes 37, no. 8 (August 1, 1988): 1071–75. http://dx.doi.org/10.2337/diabetes.37.8.1071.

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23

Imano, E., H. Kadowaki, T. Kadowaki, N. Iwama, T. Watarai, R. Kawamori, T. Kamada, and S. I. Taylor. "Two patients with insulin resistance due to decreased levels of insulin-receptor mRNA." Diabetes 40, no. 5 (May 1, 1991): 548–57. http://dx.doi.org/10.2337/diabetes.40.5.548.

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24

Kellerer, M., G. Kroder, S. Tippmer, L. Berti, R. Kiehn, L. Mosthaf, and H. Haring. "Troglitazone prevents glucose-induced insulin resistance of insulin receptor in rat-1 fibroblasts." Diabetes 43, no. 3 (March 1, 1994): 447–53. http://dx.doi.org/10.2337/diabetes.43.3.447.

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25

Ferrannini, E., S. Vichi, H. Beck-Nielsen, M. Laakso, G. Paolisso, and U. Smith. "Insulin action and age. European Group for the Study of Insulin Resistance (EGIR)." Diabetes 45, no. 7 (July 1, 1996): 947–53. http://dx.doi.org/10.2337/diabetes.45.7.947.

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26

Pedersen, O., and H. Beck-Nielsen. "Insulin Resistance and Insulin-Dependent Diabetes Mellitus." Diabetes Care 10, no. 4 (July 1, 1987): 516–23. http://dx.doi.org/10.2337/diacare.10.4.516.

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27

de Neeling, J. N. "Insulin resistance and non-insulin-dependent diabetes." JAMA: The Journal of the American Medical Association 274, no. 18 (November 8, 1995): 1426b—1426. http://dx.doi.org/10.1001/jama.274.18.1426b.

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28

de Neeling, J. Nico D. "Insulin Resistance and Non—insulin-dependent Diabetes." JAMA: The Journal of the American Medical Association 274, no. 18 (November 8, 1995): 1426. http://dx.doi.org/10.1001/jama.1995.03530180020016.

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29

Jang, Yeon Jeong. "Psychological Insulin Resistance: Key Factors and Intervention." Journal of Korean Diabetes 22, no. 3 (September 30, 2021): 192–96. http://dx.doi.org/10.4093/jkd.2021.22.3.192.

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Insulin is a mainstay of treatment in patients with type 2 diabetes mellitus to control blood sugar levels and reduce the risk of diabetes complications, but psychological insulin resistance can delay insulin treatment. Psychological insulin resistance can be defined as a negative attitude and feelings toward insulin treatment experienced by diabetics. Factors influencing psychological insulin resistance include a lack of understanding of diabetic pathophysiology, a negative attitude toward insulin treatment, anxiety about insulin therapy complications and hypoglycemia, distorted beliefs, daily constraints, fear or pain from injections, and discomfort. Various approaches to psychological insulin resistance involve direct demonstration of the insulin administration processes, education regarding diabetic pathophysiology and insulin action, assessment and evaluation of the degree of psychological insulin resistance, patient group training, building correct support systems, and providing contacts (e.g., diabetes center, diabetes nurse educator). The role of healthcare providers is important in reducing patients’ psychological insulin resistance through various interventions.

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30

Jang, Yeon Jeong. "Psychological Insulin Resistance: Key Factors and Intervention." Journal of Korean Diabetes 22, no. 3 (September 30, 2021): 192–96. http://dx.doi.org/10.4093/jkd.2021.192.196.192.

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Insulin is a mainstay of treatment in patients with type 2 diabetes mellitus to control blood sugar levels and reduce the risk of diabetes complications, but psychological insulin resistance can delay insulin treatment. Psychological insulin resistance can be defined as a negative attitude and feelings toward insulin treatment experienced by diabetics. Factors influencing psychological insulin resistance include a lack of understanding of diabetic pathophysiology, a negative attitude toward insulin treatment, anxiety about insulin therapy complications and hypoglycemia, distorted beliefs, daily constraints, fear or pain from injections, and discomfort. Various approaches to psychological insulin resistance involve direct demonstration of the insulin administration processes, education regarding diabetic pathophysiology and insulin action, assessment and evaluation of the degree of psychological insulin resistance, patient group training, building correct support systems, and providing contacts (e.g., diabetes center, diabetes nurse educator). The role of healthcare providers is important in reducing patients’ psychological insulin resistance through various interventions.

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31

Senn, J. J., P. J. Klover, I. A. Nowak, and R. A. Mooney. "Interleukin-6 Induces Cellular Insulin Resistance in Hepatocytes." Diabetes 51, no. 12 (December 1, 2002): 3391–99. http://dx.doi.org/10.2337/diabetes.51.12.3391.

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32

Spurlin, B. A., R. M. Thomas, A. K. Nevins, H. J. Kim, Y. J. Kim, H. L. Noh, G. I. Shulman, J. K. Kim, and D. C. Thurmond. "Insulin Resistance in Tetracycline-Repressible Munc18c Transgenic Mice." Diabetes 52, no. 8 (July 25, 2003): 1910–17. http://dx.doi.org/10.2337/diabetes.52.8.1910.

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33

Mikhail, Nasser. "Insulin U-500, the Practical Solution for the treatment of Patients with High Insulin Requirements." Current Diabetes Reviews 17, no. 1 (December 4, 2020): 26–29. http://dx.doi.org/10.2174/1573399816666200408084614.

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Background: Human regular insulin 500 (U-500) is 5 five times more concentrated than the traditional regular human insulin (U-100). Thus, every 1 ml of U-500 contains 500 units of insulin as opposed to 100 units/ml with most types of insulin. Methods: Review of all the relevant clinical studies related to insulin U-500 until February 12, 2020. Results: Insulin U-500 is indicated in patients with type 2 diabetes who require more than 200 units of insulin per day. Insulin U-500 has both prandial and basal actions, and can be injected as monotherapy in a convenient twice-daily regimen. Available data suggest that insulin U-500 is effective, associated with better compliance, and decreased injection pain compared with non-concentrated insulins. Its main limitations are hypoglycemia and weight gain, and the possibility of dosing errors. Conclusions: Overall, insulin U-500 is an effective and safe treatment for patients with type 2 diabetes and insulin resistance. Randomized trials are needed to compare the long-term efficacy and safety of insulin U-500 with other forms of insulin regimens.

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34

Baron, A. D. "Hemodynamic actions of insulin." American Journal of Physiology-Endocrinology and Metabolism 267, no. 2 (August 1, 1994): E187—E202. http://dx.doi.org/10.1152/ajpendo.1994.267.2.e187.

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There is accumulating evidence that insulin has a physiological role to vasodilate skeletal muscle vasculature in humans. This effect occurs in a dose-dependent fashion within a half-maximal response of approximately 40 microU/ml. This vasodilating action is impaired in states of insulin resistance such as obesity, non-insulin-dependent diabetes, and elevated blood pressure. The precise physiological role of insulin-mediated vasodilation is not known. Data indicate that the degree of skeletal muscle perfusion can be an important determinant of insulin-mediated glucose uptake. Therefore, it is possible that insulin-mediated vasodilation is an integral aspect of insulin's overall action to stimulate glucose uptake; thus defective vasodilation could potentially contribute to insulin resistance. In addition, insulin-mediated vasodilation may play a role in the regulation of vascular tone. Data are provided to indicate that the pressor response to systemic norepinephrine infusions is increased in obese insulin-resistant subjects. Moreover, the normal effect of insulin to shift the norepinephrine pressor dose-response curve to the right is impaired in these patients. Therefore, impaired insulin-mediated vasodilation could further contribute to the increased prevalence of hypertension observed in states of insulin resistance. Finally, data are presented to indicate that, via a yet unknown interaction with the endothelium, insulin is able to increase nitric oxide synthesis and release and through this mechanism vasodilate. It is interesting to speculate that states of insulin resistance might also be associated with a defect in insulin's action to modulate the nitric oxide system.(ABSTRACT TRUNCATED AT 250 WORDS)

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35

Ward, W. K., C. L. Johnston, J. C. Beard, T. J. Benedetti, J. B. Halter, and D. Porte. "Insulin resistance and impaired insulin secretion in subjects with histories of gestational diabetes mellitus." Diabetes 34, no. 9 (September 1, 1985): 861–69. http://dx.doi.org/10.2337/diabetes.34.9.861.

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36

Reaven, G. M., R. J. Brand, Y. D. Chen, A. K. Mathur, and I. Goldfine. "Insulin resistance and insulin secretion are determinants of oral glucose tolerance in normal individuals." Diabetes 42, no. 9 (September 1, 1993): 1324–32. http://dx.doi.org/10.2337/diabetes.42.9.1324.

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37

de Souza, C. J., J. H. Yu, D. D. Robinson, R. G. Ulrich, and M. D. Meglasson. "Insulin secretory defect in Zucker fa/fa rats is improved by ameliorating insulin resistance." Diabetes 44, no. 8 (August 1, 1995): 984–91. http://dx.doi.org/10.2337/diabetes.44.8.984.

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38

Tang, S., H. Le-Tien, B. J. Goldstein, P. Shin, R. Lai, and I. G. Fantus. "Decreased In Situ Insulin Receptor Dephosphorylation in Hyperglycemia-Induced Insulin Resistance in Rat Adipocytes." Diabetes 50, no. 1 (January 1, 2001): 83–90. http://dx.doi.org/10.2337/diabetes.50.1.83.

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39

Ozsahin, Akatli, Suheyl Asma, Aydana Aksoyek, Cigdem Gereklioglu, and Asli Korur. "Obesity- Insulin Resistance and Diabetes." Turkish Journal of Family Medicine & Primary Care 9, no. 2 (2015): 36. http://dx.doi.org/10.5455/tjfmpc.172673.

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40

Livingstone, C., and G. W. Gould. "Insulin Resistance in Diabetes Mellitus." Scottish Medical Journal 40, no. 2 (April 1995): 37–39. http://dx.doi.org/10.1177/003693309504000202.

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41

DeFronzo, Ralph A., and Stefano Del Prato. "Insulin resistance and diabetes mellitus." Journal of Diabetes and its Complications 10, no. 5 (September 1996): 243–45. http://dx.doi.org/10.1016/1056-8727(96)00046-3.

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42

Hadigan, Colleen. "Diabetes, insulin resistance, and HIV." Current Infectious Disease Reports 8, no. 1 (February 2006): 69–75. http://dx.doi.org/10.1007/s11908-006-0037-1.

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43

Laville, M., and J. A. Nazare. "Diabetes, insulin resistance and sugars." Obesity Reviews 10 (March 2009): 24–33. http://dx.doi.org/10.1111/j.1467-789x.2008.00562.x.

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Takano, Chika, Erika Ogawa, and Satoshi Hayakawa. "Insulin Resistance in Mitochondrial Diabetes." Biomolecules 13, no. 1 (January 7, 2023): 126. http://dx.doi.org/10.3390/biom13010126.

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Mitochondrial diabetes (MD) is generally classified as a genetic defect of β-cells. The main pathophysiology is insulin secretion failure in pancreatic β-cells due to impaired mitochondrial ATP production. However, several reports have mentioned the presence of insulin resistance (IR) as a clinical feature of MD. As mitochondrial dysfunction is one of the important factors causing IR, we need to focus on IR as another pathophysiology of MD. In this special issue, we first briefly summarized the insulin signaling and molecular mechanisms of IR. Second, we overviewed currently confirmed pathogenic mitochondrial DNA (mtDNA) mutations from the MITOMAP database. The variants causing diabetes were mostly point mutations in the transfer RNA (tRNA) of the mitochondrial genome. Third, we focused on these variants leading to the recently described “tRNA modopathies” and reviewed the clinical features of patients with diabetes. Finally, we discussed the pathophysiology of MD caused by mtDNA mutations and explored the possible mechanism underlying the development of IR. This review should be beneficial to all clinicians involved in diagnostics and therapeutics related to diabetes and mitochondrial diseases.

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Wang, Nasui, Weidong Chai, Lina Zhao, Lijian Tao, Wenhong Cao, and Zhenqi Liu. "Losartan increases muscle insulin delivery and rescues insulin's metabolic action during lipid infusion via microvascular recruitment." American Journal of Physiology-Endocrinology and Metabolism 304, no. 5 (March 1, 2013): E538—E545. http://dx.doi.org/10.1152/ajpendo.00537.2012.

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Insulin delivery and transendothelial insulin transport are two discrete steps that limit muscle insulin action. Angiotensin II type 1 receptor (AT1R) blockade recruits microvasculature and increases glucose use in muscle. Increased muscle microvascular perfusion is associated with increased muscle delivery and action of insulin. To examine the effect of acute AT1R blockade on muscle insulin uptake and action, rats were studied after an overnight fast to examine the effects of losartan on muscle insulin uptake ( protocol 1), microvascular perfusion ( protocol 2), and insulin's microvascular and metabolic actions in the state of insulin resistance ( protocol 3). Endothelial cell insulin uptake was assessed, using 125I-insulin as tracer. Systemic lipid infusion was used to induce insulin resistance. Losartan significantly increased muscle insulin uptake (∼60%, P < 0.03), which was associated with a two- to threefold increase in muscle microvascular blood volume (MBV; P = 0.002) and flow (MBF; P = 0.002). Losartan ± angiotensin II had no effect on insulin internalization in cultured endothelial cells. Lipid infusion abolished insulin-mediated increases in muscle MBV and MBF and lowered insulin-stimulated whole body glucose disposal ( P = 0.0001), which were reversed by losartan administration. Inhibition of nitric oxide synthase abolished losartan-induced muscle insulin uptake and reversal of lipid-induced metabolic insulin resistance. We conclude that AT1R blockade increases muscle insulin uptake mainly via microvascular recruitment and rescues insulin's metabolic action in the insulin-resistant state. This may contribute to the clinical findings of decreased cardiovascular events and new onset of diabetes in patients receiving AT1R blockers.

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Vargas-Uricoechea, Hernando. "Efficacy and Safety of Insulin Glargine 300 U/mL versus 100 U/mL in Diabetes Mellitus: A Comprehensive Review of the Literature." Journal of Diabetes Research 2018 (2018): 1–28. http://dx.doi.org/10.1155/2018/2052101.

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To achieve good metabolic control in diabetes and maintain it in the long term, a combination of changes in lifestyle and pharmacological treatment is necessary. The need for insulin depends upon the balance between insulin secretion and insulin resistance. Insulin is considered the most effective glucose-lowering therapy available and is required by people with type 1 diabetes mellitus to control their blood glucose levels; yet, many people with type 2 diabetes mellitus will also eventually require insulin therapy, due to the progressive nature of the disease. A variety of long-acting insulins is currently used for basal insulin therapy (such as insulin glargine, degludec, and detemir), each having sufficient pharmacodynamic and pharmacokinetic profiles to afford lower intrapatient variability and an extended duration of action. The new glargine-300 formulation was developed to have a flatter and more extended time-action profile than the original glargine-100, and these characteristics may translate into more stable and sustained glycemic control over a 24 h dosing interval. The objective of this comprehensive review was to summarize the available evidence on the clinical efficacy and safety of glargine-300 versus glargine-100 from the EDITION clinical trial program, in patients with type 1 and type 2 diabetes mellitus.

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Afzal, Muhammad Naeem. "Insulin deficient type 2 diabetics: Urgent need for enhanced research in Pakistan." Journal of Fatima Jinnah Medical University 16, no. 1 (December 14, 2022): 1–2. http://dx.doi.org/10.37018/bbvb7249.

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Type 2 diabetes is classically associated with insulin resistance stemming from obesity along with relative pancreatic dysfunction to sustain this resistance.1 In the recent past, Scandinavian researchers highlighted that a considerable proportion of type 2 diabetics are actually insulin deficient out of proportion to their insulin resistance.2 These patients were younger, had low BMI, and more deranged glycemic control. Based on sophisticated tests measuring insulin secretion and resistance, high glycemia in this group was attributed more towards decreased insulin secretion instead of insulin resistance. This was described Cluster 2 or severe insulin deficiency diabetes (SIDD) in ANDIS data.2 This data changed the perception about solitary attribute of insulin resistance in pathophysiology of type 2 diabetes, and the way we treat them on ameliorating insulin resistance predominantly. (continue reading on PDF file....)

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Carroll, P. B., and R. C. Eastman. "Insulin Resistance." Endocrinologist 1, no. 2 (April 1991): 89–97. http://dx.doi.org/10.1097/00019616-199104000-00005.

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Pocai, A., K. Morgan, C. Buettner, R. Gutierrez-Juarez, S. Obici, and L. Rossetti. "Central Leptin Acutely Reverses Diet-Induced Hepatic Insulin Resistance." Diabetes 54, no. 11 (October 25, 2005): 3182–89. http://dx.doi.org/10.2337/diabetes.54.11.3182.

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Wang, C. C. L., M. L. Goalstone, and B. Draznin. "Molecular Mechanisms of Insulin Resistance That Impact Cardiovascular Biology." Diabetes 53, no. 11 (October 25, 2004): 2735–40. http://dx.doi.org/10.2337/diabetes.53.11.2735.

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