Disease relevance of Retn

• Similarly, fasting and central administration of the adipocyte-derived factor, leptin, evoked a significant reduction in testicular resistin mRNA levels, whereas they remained unaltered in a model of diet-induced obesity [1].
• Stimulated resistin expression in white adipose of rats with bile duct ligation-induced liver cirrhosis: relationship to cirrhotic hyperinsulinemia and increased tumor necrosis factor-alpha [2].
• Further study is necessary to document the role of resistin in metabolic abnormalities of liver cirrhosis [2].
• Lowest glucose tolerances were found in HsF and particularly in LC-HsF-HP-fed animals irrespective of line, but this paralleled reduced plasma adiponectin levels, elevated plasma resistin levels, higher retroperitoneal fat masses, and reduced insulin sensitivity (indexed by insulin-induced hypoglycemia) only in Wistar rats [3].
• However, since resistin-induced satiety was modest and transient, as central administration for several days did not affect body weight, the physiological relevance and therapeutic potential of the observed principal phenomenon may be limited [4].

Psychiatry related information on Retn

• Food deprivation led to a decrease in resistin mRNA expression only in adipose tissue, not in any of the other tissues studied [5].

High impact information on Retn

• The adipose-derived hormone resistin is postulated to link obesity to insulin resistance and diabetes [6].
• Adipose-derived resistin and gut-derived resistin-like molecule-beta selectively impair insulin action on glucose production [6].
• In the presence of physiologic hyperinsulinemia, the infusion of purified recombinant resistin, increasing circulating resistin levels by approximately twofold to 15-fold, inhibited glucose metabolism such that lower rates of glucose infusion were required to maintain the plasma glucose concentration at basal levels [6].
• Glucose uptake was associated with increased expression of FDPs, including resistin ( approximately 5-fold), adiponectin ( approximately 2-fold), leptin ( approximately 15-fold), plasminogen activating inhibitor-1 ( approximately 10-fold), and angiotensinogen ( approximately 4-fold) in visceral fat, but markedly less in subcutaneous fat [7].
• However, the most dramatic increase was observed with FIZZ1 (found in inflammatory zone; also known as RELM-alpha or resistin-like molecule-alpha), which was induced 17-fold to approximately 25-fold at the peak of expression [8].

Chemical compound and disease context of Retn

• To explore this possibility, we have investigated effects of acute euglycemic (5.2+/-0.1 mmol/L) hyperinsulinemia (96+/-8 microU/mL) with and without concurrent infusion of lipid plus heparin (to raise or lower plasma free fatty acid [FFA] levels) on glucose turnover and plasma resistin levels in alert rats [9].
• Adiponectin and resistin in the neonatal rat: effects of dexamethasone and hypoxia [10].

Biological context of Retn

• Resistin gene expression was demonstrated in rat testis throughout postnatal development, with maximum mRNA levels in adult specimens [1].
• Resistin, an adipose-derived polypeptide hormone, is proposed as a candidate of insulin resistance, although its roles in inhibiting adipogenesis and in inflammation have also been suggested [2].
• Expression of the resistin transgene was detected by Northern blot analysis in adipose tissue and by real-time PCR in skeletal muscle and was associated with increased serum fatty acids and muscle triglycerides, impaired skeletal muscle glucose metabolism, and glucose intolerance in the absence of any changes in serum resistin concentrations [11].
• Lipid metabolism and resistin gene expression in insulin-resistant Fischer 344 rats [12].
• Alternative splicing generates a novel non-secretable resistin isoform in Wistar rats [13].

Anatomical context of Retn

• Resistin, a recently cloned adipose-secreted factor, is primarily involved in the modulation of insulin sensitivity and adipocyte differentiation [1].
• Overall, our present results provide the first evidence for the expression, regulation and functional role of resistin in rat testis [1].
• At this age, resistin peptide was immunodetected in interstitial Leydig cells and Sertoli cells within seminiferous tubules [1].
• Epididymal and inguinal adipose tissue and liver were collected after rats were killed and mRNA expression of SCD1 and resistin was measured [14].
• Transgenic and recombinant resistin impair skeletal muscle glucose metabolism in the spontaneously hypertensive rat [11].

Associations of Retn with chemical compounds

• From a functional standpoint, resistin, in a dose-dependent manner, significantly increased both basal and choriogonadotropin-stimulated testosterone secretion in vitro [1].
• In addition, testicular resistin mRNA was down-regulated by the selective agonist of PPARgamma, rosiglitazone, in vivo and in vitro [1].
• Adipose leptin, uncoupling protein-3 and resistin mRNAs, muscle GLUT-4, and circulating lipids were not affected by prenatal dex [15].
• Glucose intolerance and resistin expression in rat offspring exposed to ethanol in utero: modulation by postnatal high-fat diet [16].
• Resistin mRNA levels are downregulated by estrogen in vivo and in vitro [17].

Regulatory relationships of Retn

• These results implied that hyperinsulinemia and increased TNF-alpha levels might upregulate adipose resistin gene in BDL-induced liver cirrhosis [2].
• RESULTS: In fasted rats, central injection of resistin decreased food intake acutely and increased the number of cells that express Fos protein in the arcuate nucleus but not in any other hypothalamic structure [4].

Other interactions of Retn

• Leptin, adiponectin, and resistin are key hormones produced by adipose tissue [18].
• In normal control rats, in vivo insulin infusion and ex vivo administration of TNF-alpha to cultured fat pads increased resistin gene expression significantly [2].
• These results suggest testosterone to be a regulator of resistin and PRLR mRNA expression in the adipose tissue of male mice [19].
• L6 myoblasts were differentiated in 2% FBS and serum starved for 24h prior to stimulation for 24h with either insulin 1 microM (n=6), rosiglitazone 10 microM (n=6), resistin 500 nM (n=6) or the MAP kinase inhibitor PD098059 50 microM (n=6) for 30 min, followed by insulin 1 microM for 24h [20].
• We sought to determine whether resistin, a circulating adipose-derived hormone in rodents, has actions on the hypothalamus by determining the effects of central resistin injection on food intake and on hypothalamic Fos protein expression [4].

Analytical, diagnostic and therapeutic context of Retn

• The study aimed to examine resistin expression and its association with insulin and TNF-alpha in a cirrhotic rat model using bile duct ligation (BDL) [2].
• Adipocyte Retn mRNA levels were examined using northern blotting [21].
• Results of Western blotting analysis also showed that estrogen decreased adipose resistin contents in vivo and in vitro [17].
• Moreover, we studied the effect of orchidectomy and ovariectomy in rats of different ages and showed that gonadal hormones increase adipose tissue resistin mRNA expression in male rats [22].
• Subcutaneous injection of estradiol benzoate reduced resistin mRNA levels in adipocytes isolated from the inguinal, parametrial, perirenal, retroperitoneal, or periovarian fat deposits of OVX rats, while an in vitro study showed that estradiol treatment decreased resistin mRNA levels in cultured rat periovarian fat adipocytes [17].

References