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The mechanisms underlying improved insulin sensitivity after surgically-induced weight loss are still unclear. We monitored skeletal muscle metabolism in obese individuals before and over 52 weeks after metabolic surgery. Initial weight loss occurs in parallel with a decrease in muscle oxidative capacity and respiratory control ratio. Persistent elevation of intramyocellular lipid intermediates, likely resulting from unrestrained adipose tissue lipolysis, accompanies the lack of rapid changes in insulin sensitivity. Simultaneously, alterations in skeletal muscle expression of genes involved in calcium/lipid metabolism and mitochondrial function associate with subsequent distinct DNA methylation patterns at 52 weeks after surgery. Thus, initial unfavorable metabolic changes including insulin resistance of adipose tissue and skeletal muscle precede epigenetic modifications of genes involved in muscle energy metabolism and the long-term improvement of insulin sensitivity.
We review our understanding of Saturn's rings after nearly 6 years of observations by the Cassini spacecraft. Saturn's rings are composed mostly of water ice but also contain an undetermined reddish contaminant. The rings exhibit a range of structure across many spatial scales; some of this involves the interplay of the fluid nature and the self-gravity of innumerable orbiting centimeter- to meter-sized particles, and the effects of several peripheral and embedded moonlets, but much remains unexplained. A few aspects of ring structure change on time scales as short as days. It remains unclear whether the vigorous evolutionary processes to which the rings are subject imply a much younger age than that of the solar system. Processes on view at Saturn have parallels in circumstellar disks.
Die Rolle Deutschlands in der multilateralen Entwicklungszusammenarbeit unter besonderer Berücksichtigung der entwicklungspolitischen Ergebnisse des UN-Millenniumsgipfels // Klaus-Jürgen Hedrich
I. Akteure und Strukturen der multilateralen Entwicklungszusammenarbeit
II. Entwicklungspolitik der Vereinten Nationen
III. Der Milleniums-Gipfel der Vereinten Nationen
Multilaterale Organisationen und neue Formen der internationalenEntwicklungszusammenarbeit / Die Rolle Deutschlandsin der multilateralen Entwicklungszusammenarbeit —Diskussionszusammenfassung // Norman Weiß
Der Forschungskreis Vereinte Nationen veranstaltete am 25. Juni 2016 seine dreizehnte Konferenz in Kooperation mit dem „Forum internationale Ordnung“ des Auswärtigen Amtes. Die Potsdamer UNO-Konferenzen stellen in ihrem Programm traditionell eine Verbindung von Wissenschaft und Praxis her unter Beteiligung unterschiedlicher Disziplinen.
Die Konferenz 2016 widmete sich dem Thema „Die Rolle der Vereinten Nationen in der multilateralen Entwicklungszusammenarbeit“.
Entwicklung als wichtiges Ziel der Vereinten Nationen und ihrer Mitgliedstaaten ist auch für andere Handlungs- und Politikfelder wichtig. Bilanz und Ausblick, die auf der Konferenz unternommen wurden, betrafen deshalb nicht nur die Entwicklungspolitik im eigentlichen Sinne – hier standen die 2015 beschlossenen Nachhaltigkeitsziele (SDGs) zur Debatte –, sondern bezogen auch umweltpolitische und menschenrechtliche Aspekte mit ein.
Die Referate zum Thema Entwicklung wurden eingerahmt von zwei Vorträgen zu aktuellen UN-politischen Fragen: der Wahl des neuen Generalsekretärs der Vereinten Nationen in New York nach einem reformierten Wahlverfahren, das mehr Transparenz und für UN-Mitgliedstaaten und NGOs mehr Beteiligungsmöglichkeiten bietet, und die Neuorganisation innerhalb des Auswärtigen Amtes, was die Vereinten Nationen betrifft.
Mitochondria are critical for hypothalamic function and regulators of metabolism. Hypothalamic mitochondrial dysfunction with decreased mitochondrial chaperone expression is present in type 2 diabetes (T2D). Recently, we demonstrated that a dysregulated mitochondrial stress response (MSR) with reduced chaperone expression in the hypothalamus is an early event in obesity development due to insufficient insulin signaling. Although insulin activates this response and improves metabolism, the metabolic impact of one of its members, the mitochondrial chaperone heat shock protein 10 (Hsp10), is unknown. Thus, we hypothesized that a reduction of Hsp10 in hypothalamic neurons will impair mitochondrial function and impact brain insulin action. Therefore, we investigated the role of chaperone Hsp10 by introducing a lentiviral-mediated Hsp10 knockdown (KD) in the hypothalamic cell line CLU-183 and in the arcuate nucleus (ARC) of C57BL/6N male mice. We analyzed mitochondrial function and insulin signaling utilizing qPCR, Western blot, XF96 Analyzer, immunohistochemistry, and microscopy techniques. We show that Hsp10 expression is reduced in T2D mice brains and regulated by leptin in vitro. Hsp10 KD in hypothalamic cells induced mitochondrial dysfunction with altered fatty acid metabolism and increased mitochondria-specific oxidative stress resulting in neuronal insulin resistance. Consequently, the reduction of Hsp10 in the ARC of C57BL/6N mice caused hypothalamic insulin resistance with acute liver insulin resistance.
Mitochondria are critical for hypothalamic function and regulators of metabolism. Hypothalamic mitochondrial dysfunction with decreased mitochondrial chaperone expression is present in type 2 diabetes (T2D). Recently, we demonstrated that a dysregulated mitochondrial stress response (MSR) with reduced chaperone expression in the hypothalamus is an early event in obesity development due to insufficient insulin signaling. Although insulin activates this response and improves metabolism, the metabolic impact of one of its members, the mitochondrial chaperone heat shock protein 10 (Hsp10), is unknown. Thus, we hypothesized that a reduction of Hsp10 in hypothalamic neurons will impair mitochondrial function and impact brain insulin action. Therefore, we investigated the role of chaperone Hsp10 by introducing a lentiviral-mediated Hsp10 knockdown (KD) in the hypothalamic cell line CLU-183 and in the arcuate nucleus (ARC) of C57BL/6N male mice. We analyzed mitochondrial function and insulin signaling utilizing qPCR, Western blot, XF96 Analyzer, immunohistochemistry, and microscopy techniques. We show that Hsp10 expression is reduced in T2D mice brains and regulated by leptin in vitro. Hsp10 KD in hypothalamic cells induced mitochondrial dysfunction with altered fatty acid metabolism and increased mitochondria-specific oxidative stress resulting in neuronal insulin resistance. Consequently, the reduction of Hsp10 in the ARC of C57BL/6N mice caused hypothalamic insulin resistance with acute liver insulin resistance.