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Since there are in-vivo effects of growth hormone (GH) on cartilage and adipose tissue which cannot be duplicated in vitro (Salmon & Daughaday, 1957; Daughaday & Reeder, 1966; Goodman, 1968) it has been postulated that pituitary GH is modified in the body before exerting its peripheral action.
In sheep, labelled GH is altered by the kidneys and returned to the circulation in an immunologically modified form (Wallace, Stacy & Thorburn, 1969). The altered material may still be biologically active and responsible for some of the observed effects of pituitary GH. We used the fat mobilizing action of GH in sheep (Bassett & Wallace, 1966) to test whether nephrectomy had an effect on the biological activity of injected GH.
The sheep were fasted for 24 h before the start of all experiments and throughout the experimental period. Blood samples were collected into heparinized tubes from jugular cannulae inserted the day before
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mellitus and atherosclerotic cardiovascular disease ( Hubert et al . 1983 , de Marco et al . 1999 ). Fatty acids are one of the mediators of insulin resistance ( Boden 1998 ), and an imbalance in fatty acid metabolism results in the accumulation of
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PPAR ligands are certain lipids and lipid derivatives such as unsaturated fatty acids and eicosanoids, capable of activating one or more PPAR isoforms ( Hihi et al . 2002 ). Indeed, the three PPAR isotypes, named PPARα, PPARγ, and PPARδ, can be
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, Li et al . 2012 , GBD et al . 2016 , Chen et al . 2017 ). Chronic exposure to elevated saturated fatty acid (SFA) is a major risk factor for β-cell dysfunction that can accelerate the progression of T2DM ( Welsh et al . 2005 , Risérus et al
Department of Physiology, Prince Henry's Institute of Medical Research, Xiangya Medical School, Central South University, Changsha, 410078 People's Republic of China
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Introduction Pancreatic β-cells secrete insulin in response to stimulation by nutrients such as glucose and free fatty acids (FFAs). Glucose-stimulated insulin secretion (GSIS) plays an important role in maintaining glucose homeostasis. In
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steps were followed as described earlier. Measurement of liver and fecal cholesterol and fatty acids Fecal and liver total lipids were extracted from dried powdered feces using chloroform:methanol (2:1) according to the classic Folch method
Hypothalamic Integration Mechanisms, Netherlands Institute for Neuroscience, Amsterdam, The Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands
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Department of Vascular Medicine, Amsterdam Diabetes Centre, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands
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Hypothalamic Integration Mechanisms, Netherlands Institute for Neuroscience, Amsterdam, The Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands
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after preparation. To study the uptake of triglyceride-derived fatty acids, mice were fasted for 4 h and blood was drawn via the tail vein to determine BA levels (for the complete protocol, Supplementary methods, see section on supplementary data
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