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Impact of Dietary and Exercise Interventions on Brain Insulin Action and Brain Function
Published in André Kleinridders, Physiological Consequences of Brain Insulin Action, 2023
The connection between obesigenic and/or diabetogenic lifestyle factors and cognitive or emotional outcomes in humans is difficult to investigate. Some epidemiological studies and intervention trials cover hard outcomes (frequency of neurological disorders) or symptom load. Functional magnetic resonance imaging (fMRI) studies have investigated the impact of exercise, but not dietary changes. Brain-derived neurotrophic factor (BDNF) is the only biomarker related to severity and frequency of obesity, eating disorders, depression, and dementia (5–8). BDNF SNPs are risk factors for these disorders (9–14). BDNF levels are reduced by hyperglycemia, independently of insulin levels (15).
Pituitary Gland
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Muscle. GH decreases skeletal muscle glucose utilization, resulting in a diabetogenic (anti-insulin) effect. Its anabolic effects on muscle are mediated by increased amino acid uptake and enhancing protein synthesis, cell proliferation and suppression of protein breakdown.
Oxidative stress and pre-eclampsia
Published in Pankaj Desai, Pre-eclampsia, 2020
Relative insulin resistant states of late pregnancy have a vital role to play in the changes in lipid metabolism all throughout pregnancy. It is well-known that pregnancy is a diabetogenic state.7 Nevertheless, all pregnancies may not manifest clinical diabetes. This relative insulin resistance progressively increases as pregnancy advances. As soon as delivery occurs, the relatively altered insulin sensitivity is restored to normal, and the potential diabetogenic state is reversed. Insulin resistance does not clinically manifest as loss of euglycemic states in all pregnant subjects. In most pregnancies, blood sugar levels do not cross their thresholds to be labelled as overt diabetes. However the relative insulin resistance is reflected in circulating insulin levels, which are found to be consistently increasing in pregnancy. Placental growth hormone seems to have an important complementary role in this. Placental growth hormone induces maternal insulin resistance and thereby facilitates the mobilisation of maternal nutrients for foetal growth.8
N-acetyl cysteine can blunt metabolic and cardiovascular effects via down-regulation of cardiotrophin-1 in rat model of fructose-induced metabolic syndrome
Published in Archives of Physiology and Biochemistry, 2023
Azza S. Abdelhaffez, Ebtihal A. Abd El-Aziz, Maha B. Tohamy, Asmaa M. Ahmed
Metabolic syndrome (MS) is a promptly growing global pandemic. Epidemiological research reported that the prevalence of MS was approximately one-quarter of the world’s adult population (Saklayen 2018) and was estimated to affect 25% of Middle East countries population (Ansarimoghaddam et al.2018). MS is associated with a greater threat of numerous chronic pathologies comprising cardiovascular diseases and type 2 diabetes. It is characterised by a cluster of metabolic abnormalities including elevated fasting glucose, insulin resistance (IR), obesity, atherogenic dyslipidaemia, hypertension, and low-grade inflammation (Park et al.2013a). One of the main contributing operators for the development of MS is the diabetogenic food with high fructose content. It is also involved in the development of type 2 diabetes and cardiovascular diseases (Malik et al.2010). Animals nourished a high-fructose diet develop clinical features of MS such as IR, dyslipidaemia, and adiposity which may be helpful for evaluating possible curative interventions against MS (de Moura et al.2008).
Neuroprotective validation of pectin in T2DM-induced allodynia and hyperalgesia in diabetic peripheral neuropathic pain
Published in Archives of Physiology and Biochemistry, 2023
Rajnish Srivastava, Laxmi Tripathi, Sudhansu Ranjan Swain, Jagan Singh
Clearly, CSL-OP as well as standard gliclazide treatment has consistently demonstrated glucose lowering effect on (HFD) and high fat emulsion (HFE) + STZ model of T2DM and also improved peripheral pain complications. DNA alkylation induces activation of ADPribosylation, a process indispensable for the diabetogenic effect of STZ. Subsequently, depletion of NAD + and ATP secondary to poly-ribosylation in combination with donation of nitric oxide (NO) lead to generation of unstable chemical molecules including superoxide radicals which have the potential to cause damage to pancreatic β-cells. These cellular events decrease pancreatic β-cell mass via necrosis followed by decreased insulin secretion and action as well as a hyperglycaemia. However, the FRSA of the CSL-OP revealed pancreato-protective activity that can be correlated with the intact pancreatic β-cell integrity (Martini and Ursini 1996). The elevated ROS play detrimental roles in diabetic end-organ damage, particularly oxidative stress-mediated endothelial dysfunction. Nerve tissue also express aldose reductase and can be damaged by diabetic hyperglycaemia (Pari and Srinivasan 2010, Kaeidi et al.2011). (Lawrence and Roach 1997, Boye et al. 2020).
Increased pancreatic-derived factor (PANDER) levels in gestational diabetes mellitus
Published in Gynecological Endocrinology, 2019
Nadiye Koroglu, Ilkbal Temel Yuksel, Berna Aslan Cetin, Esra Nur Tola, Nura Fitnat Topbas, Ugur Turhan, Gonca Yetkin Yildirim
During the last decade, beta-cell dysfunction has been shown to be the primary determinative factor for type 2 DM [17]. Numerous mechanisms have been proposed for beta-cell dysfunction [18–20]. Increasing evidence points to the critical role of cytokines, including PANDER, that are secreted from the pancreatic islet cells during beta-cell dysfunction in type 2 DM [21]. GDM and type 2 DM share several common pathophysiological characteristics, most notably, insulin resistance [22]. Insulin resistance during pregnancy occurs due to the increased production of diabetogenic hormones, the variable production of adipocytokines, and maternal obesity. Maternal glucose intolerance occurs if insulin secretion is not increased to compensate for the insulin resistance that occurs in the second half of the pregnancy; this glucose intolerance may lead to the development of GDM, particularly in the presence of genetic and environmental factors [23]. Pancreatic beta-cell dysfunction is also involved in GDM pathophysiology [24]. Thus, we hypothesized that PANDER levels might increase during GDM. In this study, we found that PANDER levels were significantly increased in GDM patients. Increased PANDER levels might be responsible for the beta-cell dysfunction that occurs during GDM.