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Pathophysiology of Diabetes
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
In type 2 diabetes, obesity and weight gain influence insulin resistance. Though genetic determinants are present, diet, exercise, and lifestyle are extensively involved. Adipose tissues increase the plasma levels of free fatty acids, which can impair insulin-stimulated glucose transport and the activity of muscle glycogen synthase. The adipose tissues are believed to have endocrine functions. They release adipocytokines that may be metabolically favorable or unfavorable. Adiponectin is an example of a metabolically favorable adipocytokine. Unfavorable adipocytokines include IL-6, leptin, resistin, and tumor necrosis factor-alpha. Insulin resistance occurring later in life is also related to intrauterine growth restriction and low birth weight. This may be in conjunction with prenatal environmental influences upon metabolism of glucose.
Endocrine and Metabolic Side Effects
Published in Ayse Serap Karadag, Berna Aksoy, Lawrence Charles Parish, Retinoids in Dermatology, 2019
Ayse Serap Karadag, Emin Ozlu, Bodo C. Melnik
White adipose tissue acts as an endocrine organ producing a variety of hormones (adipocytokines), including adiponectin, leptin, tumor-necrosis factor alpha, and angiotensin II, which influence lipid metabolism, systemic insulin sensitivity, and inflammation. Adiponectin is the most abundant peptide secreted by adipocytes, whose reduction plays a central role in obesity-related diseases, including insulin resistance/type 2 diabetes and cardiovascular disease. In addition to adipocytes, other cell types, such as skeletal and cardiac myocytes and endothelial cells, can also produce this adipocytokine. Adiponectin performs many metabolic functions that link to energy metabolism (151,152). The hormone leptin is also a hormone predominantly secreted by adipose cells that helps to regulate energy balance by inhibiting hunger acting on receptors in the arcuate nucleus of the hypothalamus. In obesity, a decreased sensitivity to leptin occurs resulting in an inability to detect satiety despite high energy stores and high levels of leptin. The primary function of the hormone leptin is the regulation of adipose tissue mass through central hypothalamus−mediated effects on hunger, food energy use, physical exercise, and energy balance (153,154).
Metabolism in normal pregnancy
Published in Moshe Hod, Lois G. Jovanovic, Gian Carlo Di Renzo, Alberto de Leiva, Oded Langer, Textbook of Diabetes and Pregnancy, 2018
Emilio Herrera, Henar Ortega-Senovilla
Adiponectin is another adipocytokine, but unlike the foregoing examples, it increases insulin sensitivity. During normal pregnancy, no significant alterations in adiponectin levels have been found,64 but its levels negatively correlate with insulin resistance65 and they are lower in women with GDM than in control women.66 Cord blood adiponectin concentrations increase with gestational age and correlate positively with birth weights,67 suggesting a possible role in fetal adiposity and development. However, cord blood adiponectin concentrations in women with GDM are lower than in controls, and no relationship is found between this variable and neonatal fat mass or birth weight.58
Association of leptin and adiponectin levels with endometriosis: a systematic review and meta-analysis
Published in Gynecological Endocrinology, 2021
Zongquan Zhao, Yihong Wu, Hao Zhang, Xiaohong Wang, Xiangfan Tian, Yijing Wang, Zhenjuan Qiu, Lingyan Zou, Zhenyuan Tang, Min Huang
Adiponectin, an adipocytokine with adipocyte as its main source, also emanates from non-adipose tissues, such as muscles, liver and peritoneal cells [46–48]. Considering adiponectin’s properties, i.e. anti-inflammatory, anti-angiogenic, and anti-fibrotic, it may be regarded as a main source of the pathogenesis of endometriosis [18]. Findings obtained from the present study showed that, compared to controls, women with endometriosis had significantly lower adiponectin levels. Significant heterogeneity was not observed among the included studies. It has been reported that in endometriosis, the decreased adiponectin was the result of an increase in TNF-a and IL-6, which inhibited the transcription of the adiponectin gene [37]. Low adiponectin concentrations may facilitate the growth-promoting effects of estrogen [49] and insulin-like growth factor (IGF-I) on endometriosis [50]. Furthermore, the results indicated that women with advanced-stage endometriosis did not differ significantly from those with the early-stage endometriosis in terms of their adiponectin levels. Although high heterogeneity was witnessed among the included studies, the number of studies was few, thereby not performing any subgroup and meta-regression analyses. Since there is very limited data available regarding adiponectin in peritoneal fluid of endometriosis patients, further studies are required to ascertain the exact functions of this adipokine in endometriosis.
Effects of blood glucose on vaspin secretion in patients with gestational diabetes mellitus
Published in Gynecological Endocrinology, 2021
Yan Liu, Miao Gong, Suxin Liu, Yixing Pan, Yan Huo
Vaspin was first isolated from Otsuka Long-Evans Tokushima Fatty (OLETF) rats (an animal model of type 2 diabetes) by Hida et al. [6]. It was expressed mainly in the visceral adipose tissue and was a novel adipocytokine with an insulin-sensitizing effect in obesity [7]. Meanwhile, it was shown that vaspin mRNA expression- and serum vaspin levels increased when obesity and IR were the highest, and then decreased as diabetes worsened [7]. Salek-Maghsoudi et al. [15] also suggested that vaspin levels were a more reliable factor in diagnosing insulin resistance. Furthermore, Liu et al. [16] showed in vitro (rat insulinoma cells, INS-1) and in vivo (high-fat diet-fed rats) that vaspin could increase glucose-stimulated insulin secretion levels and decreased blood glucose levels. Moreover, the glucose tolerance level and insulin sensitivity of rats fed a high-fat diet improved, suggesting that serum vaspin secretion could improve the function of pancreatic islet beta cells to some extent. However, the results showed that vaspin was not significantly correlated with insulin resistance, this phenomenon was contradictory and needed to be verified by further research.
Relationship between adipocytokines and angiotensin converting enzyme gene insertion/deletion polymorphism in lean women with and without polycystic ovary syndrome
Published in Gynecological Endocrinology, 2020
Katarzyna Ożegowska, Joanna Bartkowiak-Wieczorek, Anna Bogacz, Agnieszka Seremak-Mrozikiewicz, Antoni J. Duleba, Leszek Pawelczyk
This study was designed to evaluate the role of several adipokines involved in the modulation of insulin sensitivity: adiponectin, visfatin, and apelin. Adiponectin is the most abundant cytokine produced by adipocytes and plays an important role in carbohydrate and lipid metabolism. It has anti-inflammatory and insulin sensitizing properties; levels of adiponectin are inversely related to the degree of adipocity [27–29]. Low levels of adiponectin correlate more closely with the degree of insulin resistance than with adiposity itself [30]. In several, but not all previous reports adiponectin levels were lower in women with PCOS [31–34]. Visfatin is also an adipocytokine involved in glucose homeostasis; it improves hepatic insulin sensitivity and mimics the action of insulin [35]. Levels of visfatin are increased in the presence of obesity. Several investigators found that in PCOS concentrations of visfatin were increased [36–38]; however, others found no significant difference [39,40]. Apelin is another adipocytokine playing an important role in the modulation of insulin resistance. It occurs in several isoforms, most relevant to the present study is apelin-36, due to its role in regulating glucose levels and lowering body weight [41]. Obesity is associated with increased production of apelin, thus providing a counter-regulatory mechanism protecting from the obesity-induced metabolic complications. The relationship of apelin with PCOS remains unclear; in some studies, this syndrome was associated with reduced levels of apelin, while others reported increased levels [13,42–44].