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      Reward Capacity Predicts Leptin Dynamics During Laboratory-Controlled Eating in Women as a Function of Body Mass Index.

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      Journal: Obesity (Silver Spring, Md.)
      Publisher: Wiley

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          Abstract

          The role of leptin in mesolimbic signaling of non-food-related rewards has been well established at the preclinical level, yet studies in humans are lacking. The present investigation explored the association between hedonic capacity and leptin dynamics and whether this association differed by BMI class.

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          Leptin receptor signaling in midbrain dopamine neurons regulates feeding.

          Jonathan Hommel, Richard Trinko, Robert Sears … (2006)
          The leptin hormone is critical for normal food intake and metabolism. While leptin receptor (Lepr) function has been well studied in the hypothalamus, the functional relevance of Lepr expression in the ventral tegmental area (VTA) has not been investigated. The VTA contains dopamine neurons that are important in modulating motivated behavior, addiction, and reward. Here, we show that VTA dopamine neurons express Lepr mRNA and respond to leptin with activation of an intracellular JAK-STAT pathway and a reduction in firing rate. Direct administration of leptin to the VTA caused decreased food intake while long-term RNAi-mediated knockdown of Lepr in the VTA led to increased food intake, locomotor activity, and sensitivity to highly palatable food. These data support a critical role for VTA Lepr in regulating feeding behavior and provide functional evidence for direct action of a peripheral metabolic signal on VTA dopamine neurons.
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            The cellular and molecular bases of leptin and ghrelin resistance in obesity

            Huxing Cui, Miguel López Cabanas, Kamal Rahmouni (2017)
            In obesity, individuals develop resistance to leptin and ghrelin, which have important functions in the neuroendocrine control of energy homeostasis. Here, Cui and colleagues discuss the mechanisms that lead to leptin and ghrelin resistance, and how they might be exploited as targets for the management and treatment of obesity.
            Article 0 comments Cited 150 times – based on 0 reviews     Review now
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              Cerebrospinal fluid leptin levels: relationship to plasma levels and to adiposity in humans.

              Michael W. Schwartz, Elaine R. Peskind, Murray Raskind … (1996)
              The adipocyte hormone, leptin (OB protein), is proposed to be an "adiposity signal" that acts in the brain to lower food intake and adiposity. As plasma leptin levels are elevated in most overweight individuals, obesity may be associated with leptin resistance. To investigate the mechanisms underlying brain leptin uptake and to determine whether reduced uptake may contribute to leptin resistance, we measured immunoreactive leptin levels in plasma and cerebrospinal fluid (CSF) of 53 human subjects. Leptin concentrations in CSF were strongly correlated to the plasma level in a nonlinear manner (r = 0.92; p = 0.0001). Like levels in plasma, CSF leptin levels were correlated to body mass index (r = 0.43; p = 0.001), demonstrating that plasma leptin enters human cerebrospinal fluid in proportion to body adiposity. However, the efficiency of this uptake (measured as the CSF:plasma leptin ratio) was lower among those in the highest as compared with the lowest plasma leptin quintile (5.4-fold difference). We hypothesize that a saturable mechanism mediates CSF leptin transport, and that reduced efficiency of brain leptin delivery among obese individuals with high plasma leptin levels results in apparent leptin resistance.
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                Author and article information

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                PubMed ID:: 28722317
                DOI:: 10.1002/oby.21930

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