China
Africa
Explore chapters and articles related to this topic
Endocrine Functions of Brain Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
Leptin can penetrate the BBB via a saturable transport through brain endothelia that express ObRb. Within the brain, leptin acts at multiple sites to suppress food intake and to increase energy expenditure. Leptin resistance, a state characterized by the inability of leptin to induce anorectic and metabolic effects in spite of hyperleptinemia, is a common condition in various chronic diseases, including some forms of obesity.
Genetics, Epigenetics, and Microbiome
Published in Emily Crews Splane, Neil E. Rowland, Anaya Mitra, Psychology of Eating, 2019
Emily Crews Splane, Neil E. Rowland, Anaya Mitra
Jeffrey Friedman and his colleagues (Zhang et al., 1994) identified the protein – now called leptin from Greek leptos meaning thin – that is the normal product of this gene. Hence, this genetic mutation is now designated lep-/-, and the lean littermates are lep+/+ (and heterozygous lep+/-). The lep-/- mice have normal birth weights but start to gain weight early in life; after they are weaned from their mothers, their weight gain is maintained by overeating and low physical activity. These mice also develop type 2 diabetes. In Chapter 5 we will learn about some of the physiological function(s) of leptin but, by way of a sneak preview, leptin is produced in rough proportion to the amount of body fat and acts in the brain as a signal to reduce eating. In the absence of this molecular brake, an important constraining mechanism on food intake is lost.
Central and Peripheral Modulators of Appetite and Satiety
Published in Emmanuel C. Opara, Sam Dagogo-Jack, Nutrition and Diabetes, 2019
Gabrielle Page-Wilson, Sam Dagogo-Jack
Leptin-receptor activation results in decreased expression of NPY, thereby inhibiting the powerful orexigenic effects of NPY (Ghilardi and Skoda 1997). Leptin’s action to suppress food intake is mediated through an elaborate neuronal circuitry that involves suppression of orexigenic signals (NPY, AgRP, MCH, hypocretins 1 and 2/orexins a and b) and activation of anorexigenic (α-MSH, MC4, CRH, CART) neuronal pathways (Schwartz et al. 2000). Mutations in the lep-r gene result in obesity and leptin resistance in db/db mice (Chen et al. 1996) and fa/fa rats (Phillips et al. 1996), respectively. Human lep-r mutations associated with morbid obesity have been described in a French kindred (Clement et al. 1998). Adipose tissue lep mRNA (Lonnqvist et al. 1995, Hamilton et al. 1995) and circulating leptin (Considine et al. 1996, Dagogo-Jack et al. 1996) levels are elevated in obese subjects, suggesting that obese persons are not responding optimally to the weight-regulating effects of leptin. The basis of this “leptin resistance” is unclear but may be related to alterations in circulating leptin-binding proteins (Lou et al. 2010), impaired blood-to-brain leptin delivery (Schwartz et al. 1996), or defects in leptin receptor signaling (Tartaglia et al. 1995, Bjorbaek et al. 1999, Ozcan et al. 2009, Myers et al. 2012).
The modulatory effects of irisin on asprosin, leptin, glucose levels and lipid profile in healthy and obese male and female rats
Published in Archives of Physiology and Biochemistry, 2022
Sibel Ozcan, Nazife Ulker, Ozgur Bulmus, Ahmet Yardimci, Mete Ozcan, Sinan Canpolat
Recently, the etiopathological studies on obesity have focussed on several hormones (appetite hormones, an/orexigenic peptide), which play a role in metabolism and body fat distribution (van der Klaauw 2018). There is a correlation between the aetiology of obesity and appetite hormones through stimulation of hunger/satiety signals, acting on fat metabolism or glucose homeostasis or inhibiting/adjusting appetite (Mantzoros et al. 2011). Irisin infusion could alter the hunger/satiety hormone levels (Tekin et al.2017). Leptin is predominantly secreted by adipose tissue and regulates energy balance. Although leptin reduces appetite, obese individuals with high circulating leptin levels were suggested to have resistance to leptin (Ozata et al.1999). Leptin resistance could alter leptin receptor signalling (Myers et al.2008). Exercise prevents against high-fat diet-induced leptin resistance in obesity (Carhuatanta et al.2011).
The Effect of Noninvasive Bariatric Surgery on the Levels of Certain Adipokines and Atherosclerosis Risk Factors in Patients with Metabolic Syndrome
Published in Journal of the American College of Nutrition, 2020
Agnieszka Wojciechowska-Kulik, Edyta Blus, Zbigniew Kowalczyk, Zbigniew Baj, Ewa Majewska
Among MetS patients, considerable attention has been focused on the role of adipokines such as leptin and adiponectin in the regulation of metabolism and their association with atherosclerosis (5). These hormones govern energy consumption, food intake and thermogenesis. Leptin regulates appetite and body weight by means of satiety receptors and the hypothalamus, and it is believed that the increased appetite and weight observed in obese patients is linked to so-called “leptin resistance” (6). Insulin stimulates leptin synthesis and, conversely, leptin modulates insulin secretion. Numerous studies confirm that leptin plays a role in the chronic pro-inflammatory state observed in MetS and its complications such as atherosclerosis (7). This chronic low-grade inflammatory process deteriorates the microvasculature and arteries in patients with MetS and diabetes through its influence on the endothelium, resulting in a greater risk of atherogenesis and diabetic foot syndrome (8, 9). These states, chronic inflammation and atherogenesis, are regarded as the two most harmful consequence of the increased plasma leptin level observed in people with obesity (10). They are also strongly influenced by adiponectin: an adipokine that improves glucose metabolism and has anti-inflammatory and anti-atherogenic effects, and whose level in plasma is reduced in patients with obesity (11, 12). Hence, the leptin/adiponectin ratio is used as a predictor of atherosclerosis in obese, diabetic and MetS patients (13).
Is sarcoidosis related to metabolic syndrome and insulin resistance?
Published in The Aging Male, 2020
Pinar Yıldız Gülhan, Ege Güleç Balbay, Merve Erçelik, Şeyma Yıldız, Mehmet Alper Yılmaz
Leptin is an appetite-regulating peptide hormone that is synthesized from white adipose tissue. The leptin value in the blood is directly proportional to adipose tissue [31,32]. It has been reported that leptin receptors are expressed on B and T cells and leptin has direct effects on lymphocytes. Leptin can stimulate T cell proliferation, stimulate a Th1 response, affect T cell activation, and increase phagocytic activity by activating macrophages and monocytes. In animal models, leptin deficiency has been associated with immune suppression [33]. Sarcoidosis is characterized by chronic granulomatous inflammation, which is believed to be a result of a persistent T-helper 1 polarized immune response [1]. Obesity and leptin may trigger the development of sarcoidosis by creating T Helper response.