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Hamnvik, Ole-Petter

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Hamnvik

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Ole-Petter

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Hamnvik, Ole-Petter
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    Omentin-1 levels are reduced by pharmacologic doses of leptin, but remain unaffected by energy deprivation and display no day-night variation
    (2014) Hamnvik, Ole-Petter; Thakkar, Bindiya; Chamberland, John; Aronis, Konstantinos; Schneider, Benjamin Edward; Mantzoros, Christos
    Objective: To study the day-night variation of omentin-1 levels and assess whether leptin, and/or short-and long-term energy deprivation alter circulating omentin-1 levels via cytokines. Design and Methods Omentin-1 levels were measured hourly in serum samples from six healthy men to evaluate for day-night variation. To study effects of acute energy deprivation and of leptin administration, eight healthy subjects were studied in the fasting state for 72 hours with administration of either placebo or metreleptin in physiological replacement doses. We evaluated the effect of leptin in pharmacological doses on serum omentin-1 and cytokine levels, as well as on omentin-1 levels in ex vivo omental adipose tissue, in fifteen healthy volunteers. To study the effect of chronic energy deprivation and weight loss on omentin-1 levels we followed eighteen obese subjects for 12 months who underwent bariatric surgery. Results: There is no day-night variation in omentin-1 levels. Short-term and chronic energy deprivation as well as ex vivo leptin administration and physiological replacement doses of leptin do not alter omentin-1 levels, whereas pharmacologic doses of metreleptin reduce omentin-1 levels whereas levels of TNF-α receptor II and IL-6 tend to increase. Conclusions: Omentin-1 levels are reduced by pharmacological doses of metreleptin independent of effects on cytokine levels.
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    Lack of mature lymphocytes results in obese but metabolically healthy mice when fed a high-fat diet
    (Springer Science and Business Media LLC, 2015-05-21) Liu, Xiaowen; Huh, Joo Young; Gong, Huizhi; Chamberland, John; Hamnvik, Ole-Petter; Mantzoros, Christos
    Background/Objectives: Obesity is characterized by chronic inflammation and immune dysregulation, as well as insulin resistance, but the link between obesity and adaptive immunity remains to be fully studied. Methods: To elucidate the role of adaptive immunity on body composition, glucose homeostasis, and inflammation, recombination-activating gene 1 knockout (Rag1-/-) mice, without mature T lymphocytes or B-lymphocytes, were maintained on a low (LFD) or high fat diet (HFD) for 11 weeks. Results: Rag1-/- mice fed HFD gained significantly more weight and had increased body fat compared to wild type. Downregulation of energy expenditure as well as brown fat UCP-1 and UCP-3 gene expression were noticed in HFD fed Rag1-/- mice compared to LFD. HFD mice had significantly decreased energy intake compared to LFD mice, consistent with decreased AgRP and increased POMC gene expressions in the hypothalamus. Moreover, compared to wild type, Rag1-/- mice had lower IL-4 levels, a cytokine recently found to induce browning in white adipocytes, and higher IL-12 levels in HFD fed Rag1-/- mice. Despite that HFD Rag1-/- mice were more obese, they had similar glucose, insulin, and adiponectin levels, while leptin was marginally increased. Conclusions: Mice with deficiency in adaptive immunity are obese, partly due to decreased energy expenditure, but are metabolically normal, suggesting that mature lymphocytes play necessary roles in the development of obesity-related metabolic dysregulation.
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    Leptin as a Modulator of Neuroendocrine Function in Humans
    (Yonsei University College of Medicine, 2012) Khan, Sami M.; Hamnvik, Ole-Petter; Brinkoetter, Mary; Mantzoros, Christos
    Leptin, a peptide hormone secreted by adipocytes in proportion of the amount of energy stored in fat, plays a central role in regulating human energy homeostasis. In addition, leptin plays a significant permissive role in the physiological regulation of several neuroendocrine axes, including the hypothalamic-pituitary-gonadal, -thyroid, -growth hormone, and -adrenal axes. Decreased levels of leptin, also known as hypoleptinemia, signal to the brain a state of energy deprivation. Hypoleptinemia can be a congenital or acquired condition, and is associated with alterations of the aforementioned axes aimed at promoting survival. More specifically, gonadotropin levels decrease and become less pulsatile under conditions of energy deprivation, and these changes can be at least partially reversed through leptin administration in physiological replacement doses. Similarly, leptin deficiency is associated with thyroid axis abnormalities including abnormal levels of thyrotropin-releasing hormone, and leptin administration may at least partially attenuate this effect. Leptin deficiency results in decreased insulin-like growth factor 1 levels which can be partially ameliorated through leptin administration, and leptin appears to have a much more pronounced effect on the growth of rodents than that of humans. Similarly, adrenal axis function is regulated more tightly by low leptin in rodents than in humans. In addition to congenital leptin deficiency, conditions that may be associated with decreased leptin levels include hypothalamic amenorrhea, anorexia nervosa, and congenital or acquired lipodystrophy syndromes. Accumulating evidence from proof of concept studies suggests that leptin administration, in replacement doses, may ameliorate neuroendocrine abnormalities in individuals who suffer from these conditions.