Role of leptin in energy expenditure: the hypothalamic perspective

Abstract

The adipocyte-derived hormone leptin is a peripheral signal that informs the brain about the metabolic status of an organism. Although traditionally viewed as an appetite-suppressing hormone, studies in the past decade have highlighted the role of leptin in energy expenditure. Leptin has been shown to increase energy expenditure in particular through its effects on the cardiovascular system and brown adipose tissue (BAT) thermogenesis via the hypothalamus. The current review summarizes the role of leptin signaling in various hypothalamic nuclei and its effects on the sympathetic nervous system to influence blood pressure, heart rate, and BAT thermogenesis. Specifically, the role of leptin signaling on three different hypothalamic nuclei, the dorsomedial hypothalamus, the ventromedial hypothalamus, and the arcuate nucleus, is reviewed. It is known that all of these brain regions influence the sympathetic nervous system activity and thereby regulate BAT thermogenesis and the cardiovascular system. Thus the current work focuses on how leptin signaling in specific neuronal populations within these hypothalamic nuclei influences certain aspects of energy expenditure.

Ketone ester supplementation blunts overreaching symptoms during endurance training overload

“…However, it is well established that leptin during episodes of energy deficit operates as a ‘starvation signal’ by decreasing basal energy expenditure through suppression of heart rate, blood pressure, thyroid hormone levels and sympathetic nervous system activity (Flier, ; Pandit et al . ). Thus, lower basal metabolic rate effected by a decrease in leptin (Woods et al.…”

Leptin stimulates tissue rat mast cell pro-inflammatory activity and migratory response

“…Leptin is primarily known for its role as a hypothalamic modulator of food intake, body weight, and energy expenditure [16]. Interestingly, its circulating levels closely correlate with body mass index (BMI) as well as adipose tissue mass [17].…”

Ethanol extracts of <i>Aster yomena</i> (Kitam.) Honda inhibit adipogenesis through the activation of the AMPK signaling pathway in 3T3-L1 preadipocytes

“…We further examined the influence of EEAY on the expression of adipocyte-related markers such as aP2 and leptin (9,11). As shown in Figure 3B, the increased expression of aP2 and leptin protein in differentiated 3T3-L1 cells decreased in a concentration-dependent manner compared to that in the control group after EEAY administration.…”

“…The differentiation of preadipocytes into mature adipocytes is accompanied by the sequential expression and activation of adipogenic transcription factors, including peroxisome proliferatoractivated receptor-γ (PPARγ), CCAAT/enhancer-binding proteins (C/EBPs), and sterol regulatory element-binding protein-1c (SREBP-1c) in a coordinated manner (6,7). In the final stages of the differentiation, adipocytes secrete adipose tissue-specific products, including adipocyte-specific fatty acid binding protein (aP2) and leptin (8)(9)(10)(11). After differentiation, they regulate the lipid metabolism by synthesizing lipolytic enzymes such as fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), and hormone-sensitive lipase (12,13).…”