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Protective role of mitochondrial uncoupling proteins against age-related oxidative stress in type 2 diabetes mellitus
Maša Čater, Lidija Križančić Bombek, 2022, review article

Abstract: The accumulation of oxidative damage to DNA and other biomolecules plays an important role in the etiology of aging and age-related diseases such as type 2 diabetes mellitus (T2D), atherosclerosis, and neurodegenerative disorders. Mitochondrial DNA (mtDNA) is especially sensitive to oxidative stress. Mitochondrial dysfunction resulting from the accumulation of mtDNA damage impairs normal cellular function and leads to a bioenergetic crisis that accelerates aging and associated diseases. Age-related mitochondrial dysfunction decreases ATP production, which directly affects insulin secretion by pancreatic beta cells and triggers the gradual development of the chronic metabolic dysfunction that characterizes T2D. At the same time, decreased glucose oxidation in skeletal muscle due to mitochondrial damage leads to prolonged postprandial blood glucose rise, which further worsens glucose homeostasis. ROS are not only highly reactive by-products of mitochondrial respiration capable of oxidizing DNA, proteins, and lipids but can also function as signaling and effector molecules in cell membranes mediating signal transduction and inflammation. Mitochondrial uncoupling proteins (UCPs) located in the inner mitochondrial membrane of various tissues can be activated by ROS to protect cells from mitochondrial damage. Mitochondrial UCPs facilitate the reflux of protons from the mitochondrial intermembrane space into the matrix, thereby dissipating the proton gradient required for oxidative phosphorylation. There are five known isoforms (UCP1-UCP5) of mitochondrial UCPs. UCP1 can indirectly reduce ROS formation by increasing glutathione levels, thermogenesis, and energy expenditure. In contrast, UCP2 and UCP3 regulate fatty acid metabolism and insulin secretion by beta cells and modulate insulin sensitivity. Understanding the functions of UCPs may play a critical role in developing pharmacological strategies to combat T2D. This review summarizes the current knowledge on the protective role of various UCP homologs against age-related oxidative stress in T2D.
Keywords: uncoupling proteins, reactive oxygen species, aging, age-related diseases, diabetes
Published in DKUM: 23.08.2023; Views: 340; Downloads: 23
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3.
Skeletal muscle uncoupling proteins in mice models of obesity
Lidija Križančić Bombek, Maša Čater, 2022, review article

Abstract: Obesity and accompanying type 2 diabetes are among major and increasing worldwide problems that occur fundamentally due to excessive energy intake during its expenditure. Endotherms continuously consume a certain amount of energy to maintain core body temperature via thermogenic processes, mainly in brown adipose tissue and skeletal muscle. Skeletal muscle glucose utilization and heat production are significant and directly linked to body glucose homeostasis at rest, and especially during physical activity. However, this glucose balance is impaired in diabetic and obese states in humans and mice, and manifests as glucose resistance and altered muscle cell metabolism. Uncoupling proteins have a significant role in converting electrochemical energy into thermal energy without ATP generation. Different homologs of uncoupling proteins were identified, and their roles were linked to antioxidative activity and boosting glucose and lipid metabolism. From this perspective, uncoupling proteins were studied in correlation to the pathogenesis of diabetes and obesity and their possible treatments. Mice were extensively used as model organisms to study the physiology and pathophysiology of energy homeostasis. However, we should be aware of interstrain differences in mice models of obesity regarding thermogenesis and insulin resistance in skeletal muscles. Therefore, in this review, we gathered up-to-date knowledge on skeletal muscle uncoupling proteins and their effect on insulin sensitivity in mouse models of obesity and diabetes.
Keywords: uncoupling protein, skeletal muscle, insulin, diabetes, obesity
Published in DKUM: 10.08.2023; Views: 351; Downloads: 20
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4.
Individualizacija avtogenega treninga za zniževanje anksioznosti s pomočjo metode biofeedback, temelječe na spremljanju variabilnosti srčne frekvence : magistrsko delo
Urška Drofenik, 2022, master's thesis

Abstract: Biofeedback, temelječ na variabilnosti srčne frekvence (HRV biofeedback), neposredno spodbuja barorefleks, respiratorno sinusno aritmijo, parasimpatično aktivnost in stimulira različne homeostatične reflekse. Pri HRV biofeedbacku se ljudi uči počasnega dihanja pri njihovi resonančni frekvenci, ki se giblje med 6,5 in 4,5 dihalnimi ciklusi na minuto. Raziskave ugotavljajo, da naj bi tako dihanje pomagalo pri spoprijemanju s stresom in zniževanju anksioznosti. Namen naše magistrske naloge je bil preučiti učinkovitost avtogenega treninga na zniževanje anksioznosti, če mu dodamo HRV biofeedback. Na vzorcu 47 udeležencev, ki smo jih razdelili v dve skupini, smo preverjali, ali prihaja do razlik, če eno skupino naučimo dihanja pri njihovi specifični resonančni frekvenci, medtem ko so v kontrolni skupini udeleženci dihali s 5,5 dihalnimi ciklusi na minuto. Vsi udeleženci so prilagojen avtogeni trening izvajali dnevno v obdobju dveh tednov. Rezultati so pokazali, da je po intervenciji prišlo do pomembnega znižanja anksioznih simptomov pri obeh skupinah, ni pa prišlo do razlik med samima skupinama. Prav tako nismo zabeležili spremembe v variabilnost srčne frekvence pri udeležencih. Kljub temu naša intervencija omogoča enostavno prilagoditev različnih tehnik sproščanja s kombinacijo počasnega dihanja v območju resonančne frekvence, kar lahko učinkovito znižuje anksioznost pri subklinični skupini posameznikov.
Keywords: anksioznost, biofeedback, variabilnost srčne frekvence, avtogeni trening
Published in DKUM: 14.02.2022; Views: 1208; Downloads: 184
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SNAP-25b-deficiency increases insulin secretion and changes spatiotemporal profile of $Ca^{2+}$ oscillations in $\beta$ cell networks
Teresa Daraio, Lidija Križančić Bombek, Marko Gosak, Ismael Valladolid-Acebes, Maša Skelin, Essam Refai, Per-Olof Berggren, Kerstin Brismar, Marjan Rupnik, Christina Bark, 2017, original scientific article

Abstract: SNAP-25 is a protein of the core SNARE complex mediating stimulus-dependent release of insulin from pancreatic $\beta$ cells. The protein exists as two alternatively spliced isoforms, SNAP-25a and SNAP-25b, differing in 9 out of 206 amino acids, yet their specific roles in pancreatic $\beta$ cells remain unclear. We explored the effect of SNAP-25b-deficiency on glucose-stimulated insulin release in islets and found increased secretion both in vivo and in vitro. However, slow photo-release of caged $Ca^{2+}$ in $\beta$ cells within pancreatic slices showed no significant differences in $Ca^{2+}$-sensitivity, amplitude or rate of exocytosis between SNAP-25b-deficient and wild-type littermates. Therefore, we next investigated if $Ca^{2+}$ handling was affected in glucose-stimulated [beta] cells using intracellular $Ca^{2+}$-imaging and found premature activation and delayed termination of [$Ca^{2+}$] i elevations. These findings were accompanied by less synchronized $Ca^{2+}$-oscillations and hence more segregated functional $\beta$ cell networks in SNAP-25b-deficient mice. Islet gross morphology and architecture were maintained in mutant mice, although sex specific compensatory changes were observed. Thus, our study proposes that SNAP-25b in pancreatic [beta] cells, except for participating in the core SNARE complex, is necessary for accurate regulation of $Ca^{2+}$-dynamics.
Keywords: insulin secretion, pre-diabetes
Published in DKUM: 23.08.2017; Views: 1404; Downloads: 199
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