Journal of Yeungnam Medical Science

Original article

Evaluation of periodontal status in women with polycystic ovary syndrome versus healthy women: a cross-sectional study: Sandhya Pavankumar, Pavan Kumar Yellarthi, Sandeep JN, Ramanarayana Boyapati, Trinath Kishore Damera, Naveen Vital Kumar G; J Yeungnam Med Sci. 2023;40(Suppl):S17-S22. Published online May 8, 2023; DOI: https://doi.org/10.12701/jyms.2023.00143

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Abstract PDF: Background
Polycystic ovary syndrome (PCOS) affects approximately 4% to 12% of females of reproductive age. Previous studies have shown an association between systemic and periodontal diseases. This study aimed to compare the prevalence of periodontal disease in women with PCOS and healthy women.
Methods
A total of 196 women aged 17 to 45 years were included in this study. Oral hygiene index-simplified (OHI-S), gingival index (GI), community periodontal index (CPI), and loss of attachment (LA) were assessed. Individuals who smoked, were pregnant, had any systemic disease (such as type 1 or type 2 diabetes mellitus, cardiovascular disease, malignancy, osteoporosis, and thyroid dysfunction), had a history of systemic antibiotic use in the past three months, or received any periodontal intervention in the past 6 months of screening were excluded. Student t-test was used to analyze the data. A p-value of <0.05 was considered statistically significant.
Results
Despite similar OHI-S scores (p=0.972) in the two groups, women with PCOS had significantly higher GI, CPI, and LA scores than healthy women (p<0.001).
Conclusion
Periodontal disease was more prevalent in women with PCOS than in healthy women. This finding may be due to the synergistic effects of PCOS and periodontitis on proinflammatory cytokines. PCOS may have an effect on periodontal disease, and vice versa. Hence, education on periodontal health and early detection and intervention for periodontal diseases is of paramount importance in patients with PCOS.

Review article

Can antioxidants be effective therapeutics for type 2 diabetes?: Soyoung Park, So-Young Park; Yeungnam Univ J Med. 2021;38(2):83-94. Published online October 8, 2020; DOI: https://doi.org/10.12701/yujm.2020.00563

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The global obesity epidemic and the growing elderly population largely contribute to the increasing incidence of type 2 diabetes. Insulin resistance acts as a critical link between the present obesity pandemic and type 2 diabetes. Naturally occurring reactive oxygen species (ROS) regulate intracellular signaling and are kept in balance by the antioxidant system. However, the imbalance between ROS production and antioxidant capacity causes ROS accumulation and induces oxidative stress. Oxidative stress interrupts insulin-mediated intracellular signaling pathways, as supported by studies involving genetic modification of antioxidant enzymes in experimental rodents. In addition, a close association between oxidative stress and insulin resistance has been reported in numerous human studies. However, the controversial results with the use of antioxidants in type 2 diabetes raise the question of whether oxidative stress plays a critical role in insulin resistance. In this review article, we discuss the relevance of oxidative stress to insulin resistance based on genetically modified animal models and human trials.

Citations

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Reviews

The relationship between muscle mitochondrial nutritional overloading and insulin resistance: Jae Han Jeon, Jun Sung Moon, Kyu Chang Won, In Kyu Lee; Yeungnam Univ J Med. 2017;34(1):19-28. Published online June 30, 2017; DOI: https://doi.org/10.12701/yujm.2017.34.1.19

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Abstract PDF: The incidence of type 2 diabetes mellitus and insulin resistance is growing rapidly. Multiple organs including the liver, skeletal muscle and adipose tissue control insulin sensitivity coordinately, but the mechanism of skeletal muscle insulin resistance has not yet been fully elucidated. However, there is a growing body of evidence that lipotoxicity induced by mitochondrial dysfunction in skeletal muscle is an important mediator of insulin resistance. However, some recent findings suggest that skeletal mitochondrial dysfunction generated by genetic manipulation is not always correlated with insulin resistance in animal models. A high fat diet can provoke insulin resistance despite a coordinate increase in skeletal muscle mitochondria, which implies that mitochondrial dysfunction is not mandatory in insulin resistance. Furthermore, incomplete fatty acid oxidation by excessive nutrition supply compared to mitochondrial demand can induce insulin resistance without preceding impairment of mitochondrial function. Taken together we suggested that skeletal muscle mitochondrial overloading, not mitochondrial dysfunction, plays a pivotal role in insulin resistance.

Obesity and Insulin Resistance in Childhood.: Kwang Hae Choi; Yeungnam Univ J Med. 2012;29(2):73-76. Published online December 31, 2012; DOI: https://doi.org/10.12701/yujm.2012.29.2.73

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Abstract PDF: More and more children are becoming obese and overweight due to several factors that include a high energy density in the diet (a high fat intake) and low energy expenditure. Consequently childhood obesity is becoming a significant health problem. Fat tissue releases many cytokines such as resistin, tumor necrosis factor-alpha, leptin, interleukin-6. These adipocytokines induce obesity-related insulin resistance. Insulin resistance is a key component of obesity-related metabolic problems such as hypertension, type 2 diabetes mellitus, dyslipidemia, non-alcoholic steatohepatitis, acanthosis nigricans and polycystic ovarian syndrome. This review article focused on insulin resistance and its related metabolic diseases.

Original Articles

Effect of Acutely Increased Glucose Uptake on Insurin Sensitivity in Rats.: Yong Woon Kim, Youl In Ma, Suck Kang Lee; Yeungnam Univ J Med. 1997;14(1):53-66. Published online June 30, 1997; DOI: https://doi.org/10.12701/yujm.1997.14.1.53

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Abstract PDF: Insulin resistance is a prominent feature of diabetic state and has heterogeneous nature. However, the pathogenetic sequence of events leading to the emergence of the defect in insulin action remains controversial. It is well-known that prolonged hyperglycemia and hyperinsulinemia are one of the causes of development of insulin resistance, but both hyperglycemia and hyperinsulinemia stimulate glucose uptake in peripheral tissue. Therefore, it is hypothesized that insulin resistance may be generated by a kind of protective mechanism preventing cellular hypertrophy. In this study, to evaluate whether the acutely increased glucose uptake inhibits further glucose transport stimulated by insulin, insulin sensitivity was measured after preloaded glucose infusion for 2 hours at various conditions in rats. And also, to evaluate the mechanism of decreased insulin sensitivity, insulin receptor binding affinity and glucose transporter 4 (GLUT4) protein of plasma membrane of gastrocnemius muscle were assayed after hyperinsulinemic euglycemic clamp studies. Experimental animals were divided into five groups according to conditions of preloaded glucose infusion: group I, basal insulin (14+/-1.9 micronU/ml) and basal glucose (75+/-0.7 mg/dl), by normal saline infusion; group II, normal insulin (33+/-3.8 micronU/ml) and hyperglycemia (207+/-6.3 mg/dl), by somatostatin and glucose infusion; group III, hyperinsulinemia (134+/-34.8 micronU/ml) and hyperglycemia (204+/-4.6 mg/dl), by glucose infusion; IV, supramaximal insulin (100+/-2.2 mg/dl), by insulin and glucose infusion; group V, supramaximal insulin(4813+/-687.9 micronU/ml) and hyperglycemia (233+/-3.1 mg/dl), by insulin and glucose infusion. Insulin sensitivity was assessed with hyperinsulinemic euglycemic clamp technique. The amounts of preloaded glucose infusion(gm/kg) were 1.88+/-0.151 in group II, 2.69+/-0.239 in group III, 3.54+/-0.198 in groupIV, and 4.32+/-0.621 in group V. Disappearance rates of glucose (Rd, mg/kg/min) at steady state of hyperinsulinemic euglycemic clamp studies were 16.9+/-3.88 in group I, 13.5+/-1.05 in group II, 11.2+/-1.17 in group III, 13.2+/-2.05 in group IV, and 10.4+/-1.01 in group V. A negative correlation was observed between amount of preloaded glucose and Rd )r=-0.701, p<0.001) when all studies were combined. Insulin receptor binding affinity and content of GLUT4 were not significantly different in all experimental groups. These results suggest that increased glucose uptake may inhibit further glucose transport and lead to decreased insulin sensitivity.

Insulin Resistance in Late Pregnant Rats.: Myung Heup Chun, Yong Woon Kim, So Young Park, Jong Yeon Kim, Suck Kang Lee; Yeungnam Univ J Med. 1995;12(2):319-330. Published online December 31, 1995; DOI: https://doi.org/10.12701/yujm.1995.12.2.319

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Abstract PDF: The influence of normal late pregnancy on insulin action and insulin secretion was studied in the Sprague-Dawley female rats. On 20th day after mating, intravenous glucose tolerance test(IVGTI) was performed in non pregnant control and pregnant rats. As results of IVGTT, glucose disappearance rate was not significantly different in both groups, but secretory response of insulin was significantly(p<0.05) increased in pregnant rat. And the ratio of insulin/ .glucose was significantly higher in pregnant rats, which means existence of insulin resistance. These insulin resistance was overcomed by increased secretory response of pancreatic insulin. Insulinogenic index( A insulin/glucose - 5 min) was highly significantly (r=0.62, p<0.01) correlated with progesterone concentration. Glycogen level and amounts of "C-glucose incorporated into glycogen after IVGTT were significantly(p<0. 05) decreased in the liver, but were not changed significantly in soleus. Glycogen synthase activity of soleus and liver was not differ significantly in the both groups. Insulin binding at varying concentrations of insulin to crude membrane of pregnant liver was not significantly different from control. In conclusions, although these pregnant rats were normal glucose tolerance due to increased secretory response of insulin, that was correlated with progesterone concentration, pregnant rat had insulin resistance. The mechanisms of insulin resistance were not related to defect of insulin binding phase and glycogen synthase, but suggest pre-receptor and/or postreceptor phase.

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