Effect of insulin on immunological phagocytosis by macrophages

Ao, Lima; Queiroz, Mary L.S.; Hm, Bräscher; Vargens, J. R.

doi:10.1007/bf01917915

Cited by 10 publications

(5 citation statements)

References 12 publications

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“…When Lima etal. [137] used insulin in physiological doses (10 -9 to 10 -a3 mol/1), they found enhancement of phagocytic responses by murine peritoneal macrophages, a result confirmed by Kragballe et al [138] using human monocytes. Using a different assay Bar et al [139] reported inhibition of antibody-dependent cellular cytotoxicity by insulin (10 -1~ mol/1), but the inhibition was not dramatic (about 30%).…”

Section: Effects Of Insulin On In Vitro Immune Functionmentioning

confidence: 68%

“…Further evidence that insulin can affect the function of the immune system comes from a variety of in vitro experiments (Table6) [136][137][138][139][140][141][142][143][144][145][146][147][148]. Rhodes [136] reported that insulin inhibited the expression of Fc receptors on guinea pig macrophages as measured by an erythrocyteantibody rosetting assay, but the concentration of insulin employed was in the 5 x 10 -5 mol/1 range; this is three to seven orders of magnitude larger than the concentration commonly regarded as physiological [137][138][139]. Similarly, Hunt and Eardley [148] reported inhibition of antibody formation and Interleukin-2-induced proliferation by these concentrations of insulin.…”

Section: Effects Of Insulin On In Vitro Immune Functionmentioning

confidence: 99%

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Multiple immunological abnormalities in patients with Type 1 (insulin-dependent) diabetes mellitus

1987

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Section: Effects Of Insulin On In Vitro Immune Functionmentioning

confidence: 68%

Section: Effects Of Insulin On In Vitro Immune Functionmentioning

confidence: 99%

Multiple immunological abnormalities in patients with Type 1 (insulin-dependent) diabetes mellitus

1987

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“…It is known that TB affects the production of insulin and that it is detrimental to insulin sensitivity [ 71 ]. Although several studies have shown the role of insulin in cellular metabolism and phagocytosis of M. tuberculosis, little is known about insulin resistance as a potential risk factor for active TB [ 72 , 73 ]. Chao et al investigated the immunological mechanisms underlying the susceptibility of diabetic patients to TB [ 74 ].…”

Section: Sensitivity Of Asian People With Dm To Tbmentioning

confidence: 99%

Diabetes and pulmonary tuberculosis: a global overview with special focus on the situation in Asian countries with high TB-DM burden

Zheng

Gao

2017

Global Health Action

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Background: The double burden of tuberculosis (TB) and diabetes mellitus (DM) is hitting certain Asian countries harder than other areas. In a global estimate, 15% of all TB cases could be attributable to DM, with 40% of those cases coming from India and China. Many other countries of South, East, and South-East Asia are of particular concern given their TB burdens, large projected increases in DM prevalence, and population size. Objective: In this narrative review, we aimed to: (i) give an overall insight into the evidence on TB-DM epidemiology from high double burden Asian countries, (ii) present the evidence on bi-directional screening implementation in this region, (iii) discuss possible factors related to higher TB susceptibility of Asian diabetic patients, and (iv) identify TB-DM comorbidity treatment challenges. Methods: The PubMed and Google Scholar databases were searched for all studies addressing DM/TB epidemiology, bi-directional screening and management in South, East and South-East Asia. Results: We identified the DM prevalences among TB patients as ranging from approximately 5% to more than 50%, whereas TB prevalences among diabetic patients were 1.8–9.5 times higher than in the general population in developing Asian countries. Evidence from studies designed to address diagnosis and treatment of the dual disease in these critical regions is scarce as well as the evidence related to possible DM patients’ genetic and acquired predisposition for TB. Conclusion: More prospective studies specifically designed to address adequate screening techniques, identify patients at risk, and define an adequate treatment of dual disease in this region are needed without delay.

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“…The phagocytic activity is low in type 2 diabetes and improves after metabolic improvement [71]. Insulin inhibits phagocytosis of normal human neutrophils [72]. It also enhances immunological phagocytosis by macrophages [72].…”

Section: Peptide Hormonesmentioning

confidence: 99%

“…Insulin inhibits phagocytosis of normal human neutrophils [72]. It also enhances immunological phagocytosis by macrophages [72]. Glucagon and somatostatin stimulated macrophage phagocytosis [70].…”

Section: Peptide Hormonesmentioning

confidence: 99%

Is there a hormonal regulation of phagocytosis at unicellular and multicellular levels? A critical review

Csaba

2017

AMicr

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Phagocytosis is an ancient cell function, which is similar at unicellular and multicellular levels. Unicells synthesize, store, and secrete multicellular (mammalian) hormones, which influence their phagocytosis. Amino acid hormones, such as histamine, serotonin, epinephrine, and melatonin stimulate phagocytosis, whereas peptide hormones, such as adrenocorticotropic hormone (ACTH), insulin, opioids, arginine vasopressin, and atrial natriuretic peptide decreased it, independently on their chemical structure or function in multicellulars. Macrophage phagocytosis of multicellulars is also stimulated by amino acid hormones, such as histamine, epinephrine, melatonin, and thyroid hormones, however, the effect of peptide hormones is not uniform: prolactin, insulin, glucagon, somatostatin, and leptin have positive effects, whereas ACTH, human chorionic gonadotropin, opioids, and ghrelin have negative ones. Steroid hormones, such as estrogen, hydrocortisone, and dexamethasone are stimulating macrophage phagocytosis, whereas progesterone, aldosterone, and testosterone are depressing it. Considering the data and observations there is not a specific phagocytosis hormone, or a hormonal regulation of phagocytosis neither unicellular, nor multicellular level, however, hormones having specific functions in multicellulars also influence phagocytosis at both levels universally (in unicellulars) or individually (in macrophages). Nevertheless, the hormonal influence cannot be neglected, as phagocytosis (as a function) is rather sensitive to minute dose of hormones and endocrine disruptors. The hormonal influence of phagocytosis by macrophages can be deduced to the events at unicellular level.

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Effect of insulin on immunological phagocytosis by macrophages

Cited by 10 publications

References 12 publications

Multiple immunological abnormalities in patients with Type 1 (insulin-dependent) diabetes mellitus

Multiple immunological abnormalities in patients with Type 1 (insulin-dependent) diabetes mellitus

Diabetes and pulmonary tuberculosis: a global overview with special focus on the situation in Asian countries with high TB-DM burden

Is there a hormonal regulation of phagocytosis at unicellular and multicellular levels? A critical review

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