Erratum: Adiponectin acts in the brain to decrease body weight

Qi, Yong; Takahashi, Nobuhiko; Hileman, Stanley M.; Patel, Hiralben R.; Berg, Anders H.; Pajvani, Utpal B.; Scherer, Philipp E.; Ahima, Rexford S.

doi:10.1038/nm0604-649a

Cited by 5 publications

(5 citation statements)

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“…Authors of previous studies have suggested that unique properties of human milk, such as leptin and adiponectin, might be biological mechanisms in reducing the risk of obesity. [27][28][29] Another possible mechanism is the ability of breastfed infants to self-regulate their energy intake to balance their energy needs. It has been proposed that infants are born with some ability to regulate their energy intake in response to internal appetite cues.…”

Section: Discussionmentioning

confidence: 99%

Do Infants Fed From Bottles Lack Self-regulation of Milk Intake Compared With Directly Breastfed Infants?

2010

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Section: Discussionmentioning

confidence: 99%

Do Infants Fed From Bottles Lack Self-regulation of Milk Intake Compared With Directly Breastfed Infants?

2010

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“…There is also the possibility that, in addition to its protective actions, adiponectin has direct harmful effects, which could be more operative in older individuals. Indeed, adiponectin has increased energy expenditure through direct actions in the central nervous system in mice (52), an effect that, if present in humans, could be particularly deleterious in older adults by potentially accelerating sarcopenia. Notable, in our study age was not an effect modifier of the association of adiponectin with incident CHD.…”

Section: Discussionmentioning

confidence: 99%

Associations of Adiponectin and Leptin with Incident Coronary Heart Disease and Ischemic Stroke in African Americans: The Jackson Heart Study

Bidulescu¹,

Liu²,

Chen³

et al. 2013

Front. Public Health

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Background: Because the predictive significance of previously reported racial differences in leptin and adiponectin levels remains unclear, we assessed the prospective association of these adipokines with the risk of cardiovascular disease (CVD) events in African Americans, a population with a high prevalence of cardiometabolic risk factors.Methods: Serum specimens from 4,571 Jackson Heart Study participants without prevalent CVD at baseline examination (2000–2004) were analyzed for adiponectin and leptin levels. Cox proportional hazard regression models were used to estimate the associations of the two adipokines with incident coronary heart disease (CHD) and incident ischemic stroke.Results: During 6.2 years average of follow-up, 98 incident CHD and 87 incident ischemic stroke events were documented. Among study participants (64% women; mean age 54 ± 13 years), the mean (standard deviation, SD) was 6.04 (4.32) μg/mL in women and 4.03 (3.14) μg/mL in men for adiponectin and 37.35 (23.90) ng/mL in women and 11.03 (10.05) ng/mL in men for leptin. After multivariable adjustment that included age, body mass index, high-density lipoprotein cholesterol, triglycerides, C-reactive protein, insulin resistance by homeostasis model assessment for insulin resistance, systolic blood pressure, hypertension medication, smoking, and physical activity, adiponectin was directly associated in women with incident stroke, HR = 1.41 (1.04–1.91) per one SD increase (p = 0.03), but not in men (p = 0.42). It was not associated with incident CHD in women or men. Leptin was not associated with incident CHD or incident stroke.Conclusion: In the largest community-based African American cohort, adiponectin was associated among women with a higher risk of incident stroke. Whether adiponectin harbors harmful properties, or it is produced in response to vascular inflammation to counter the atherosclerotic process, or the putative “adiponectin resistance” phenomenon acts, should be further assessed.

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“…Hormones derived from the pancreas, as pancreatic polypeptide (PP) (6), glucagon (7), insulin (8), and amylin (9), also exhibit anorexigenic actions. Finally, adipose tissue-derived anorexigenic signals, such as leptin (10), adiponectin (11), and resistin (12) have been described. On the other hand, gut-derived ghrelin is the only example of a peripheral hormone with orexigenic actions (13, 14), thereby increasing appetite upon its release usually before meals.…”

Section: Appetite Regulation: From the Periphery To The Hypothalamusmentioning

confidence: 99%

Glutamate and GABA in Appetite Regulation

Delgado¹

2013

Front. Endocrinol.

104

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Appetite is regulated by a coordinated interplay between gut, adipose tissue, and brain. A primary site for the regulation of appetite is the hypothalamus where interaction between orexigenic neurons, expressing Neuropeptide Y/Agouti-related protein, and anorexigenic neurons, expressing Pro-opiomelanocortin cocaine/Amphetamine-related transcript, controls energy homeostasis. Within the hypothalamus, several peripheral signals have been shown to modulate the activity of these neurons, including the orexigenic peptide ghrelin and the anorexigenic hormones insulin and leptin. In addition to the accumulated knowledge on neuropeptide signaling, presence and function of amino acid neurotransmitters in key hypothalamic neurons brought a new light into appetite regulation. Therefore, the principal aim of this review will be to describe the current knowledge of the role of amino acid neurotransmitters in the mechanism of neuronal activation during appetite regulation and the associated neuronal-astrocytic metabolic coupling mechanisms. Glutamate and GABA dominate synaptic transmission in the hypothalamus and administration of their receptors agonists into hypothalamic nuclei stimulates feeding. By using 13C High-Resolution Magic Angle Spinning Nuclear Magnetic Resonance spectroscopy based analysis, the Cerdán group has shown that increased neuronal firing in mice hypothalamus, as triggered by appetite during the feeding-fasting paradigm, may stimulate the use of lactate as neuronal fuel leading to increased astrocytic glucose consumption and glycolysis. Moreover, fasted mice showed increased hypothalamic [2-13C]GABA content, which may be explained by the existence of GABAergic neurons in key appetite regulation hypothalamic nuclei. Interestingly, increased [2-13C]GABA concentration in the hypothalamus of fasted animals appears to result mainly from reduction in GABA metabolizing pathways, rather than increased GABA synthesis by augmented activity of the glutamate-glutamine-GABA cycle.

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Erratum: Adiponectin acts in the brain to decrease body weight

Cited by 5 publications

References 0 publications

Do Infants Fed From Bottles Lack Self-regulation of Milk Intake Compared With Directly Breastfed Infants?

Do Infants Fed From Bottles Lack Self-regulation of Milk Intake Compared With Directly Breastfed Infants?

Associations of Adiponectin and Leptin with Incident Coronary Heart Disease and Ischemic Stroke in African Americans: The Jackson Heart Study

Glutamate and GABA in Appetite Regulation

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