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Gastric leptin
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2006Systematic Review
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Cammisotto PG and Bendayan M -
Systemic leptin has been shown to have a central
role in obesity, diabetes, cardiovascular and
gastrointestinal diseases. In obese patients, subcutaneous
and visceral adipose tissue overexpress leptin mRNA
(Lonnqvist et al., 1995). In long term, hyperleptinemia
results in central and peripheric leptin resistance. Central
resistance lead to hyperhagia (Munzberg and Myers,
2005) while peripheral leptin resistance has been linked
to a decrease in glucose uptake, decrease in glycogen
synthesis and accumulation of intracellular lipids leading
to peripheric insulin resistance (Liu et al., 1997; Unger,
2004). Leptin is also involved in hypertension,
arteriosclerosis, cancer and eating disorders (Ramos et
al., 2004; Chan and Mantzoros, 2005; Luo et al., 2005;
Singhal, 2005).
Gastric leptin is involved in immunity and
inflammation of the digestive tract. Helicobacter pylori,
the major cause of chronic gastritis and peptic ulcer
diseases (Blaser, 1990), increases the expression of
leptin mRNA and leptin secretion by the gastric mucosa.
In turn, leptin could stimulate monocytes to produce
proinflammatory cytokines like IL-1, IL-6 and tumour
necrosis factor α (TNF-α) (Santos-Alvarez et al., 1999;
Nishi et al., 2005). In the intestinal mucosa, leptin
modulates the activation and proliferation of T
lymphocytes and redirects cytokine responses towards a
T helper 1 phenotype by enhancing production of IL-2
and interferon (Lord et al., 2002). This seems
particularly important in inflammatory bowel diseases
that are characterized by hyperleptinemia and overactivation of the immune system. Indeed, mesenteric
adipose tissue gets hypertrophied in Crohn’s disease and
releases large amounts of leptin into the blood enteric Adipose and gastric leptin circulation (Karmiris et al., 2005; Otero et al., 2005). In
ulcerative colitis, a certain population of colonic cell
differentiates into leptin-secreting cell which have been
shown to be involved in colonic inflammation
(Siegmund et al., 2004). - Organism: Humans
- Notable Magnitude of Effect.
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1999
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Santos-Alvarez J, et al. -
«The Ob gene product, leptin, is an adipocyte-secreted hormone that centrally regulates weight control. However, leptin receptor is expressed not only in the central nervous system, but also in other systems such as reproductive and hematopoietic tissues. Human leptin has previously been shown to enhance cytokine production by murine peritoneal macrophages. In this paper we show that human leptin stimulates proliferation in a dose-dependent manner and functionally activates human circulating monocytes in vitro, by inducing the production of cytokines such as TNF-alpha and IL-6. Proliferation was assessed both by [3H]thymidine and bromodeoxyuridine incorporation at 48 h. We also checked the leptin stimulated monocyte expression of activation markers by flow cytometry: CD25, HLA-DR, CD38, CD71, CD11b, and CD11c expression increased after 72 h. Moreover, leptin increases the expression of the early activation marker CD69 in monocytes but not in lymphocytes. The stimulation produced by leptin is comparable to that produced by endotoxin [lipopolysaccharide (LPS)]. In addition, leptin can potentiate the stimulatory effect of LPS or PMA. Furthermore, we studied cytokine production (TNF-alpha and IL-6) simultaneously by flow cytometric detection of intracellular cytokines in the activated monocytes. Leptin produced a dose-dependent increase in the number of activated monocytes producing cytokines. These data indicate that leptin is a potent stimulatory hormone on human peripheral blood monocytes and suggest that it may have a role as a proinflammatory cytokine.»
- Organism: In vitro
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