Effect of obesity and insulin on immunity in non-insulin-dependent diabetes mellitus

Abstract

Objective: To understand the effect of obesity and insulin on immune functions in non-insulin-dependent diabetes mellitus (NIDDM). Subject: Fourteen obese NIDDM (body mass index (BMI) ¼ 30.6 AE 1.1), seven non-obese NIDDM (BMI ¼ 24.2 AE 0.5) and five obese non-NIDDM (BMI ¼ 28.3 AE 0.67). Interventions: We first examined the influence of insulin on the proliferation of several human cell lines. Second, we compared several immune functions between obese and non-obese NIDDM, and obese non-NIDDM patients using peripheral blood mononuclear cells. Result: Insulin decreased proliferation of T-cell lines but not that of other types of cell lines. Furthermore, obesity augmented the production of IL-1b which could have cytotoxity against islet b cells in NIDDM. Conclusion: Our data suggested that the pathophysiology of NIDDM could be affected by the change of immunity due to obesity, and the treatment of obesity in NIDDM may be important from an immunological aspect.

Systemic immunity of obese-diabetes model (db/db) mice

“…The infiltration of macrophages into the adipose tissue observed in the obese state worsens the inflammatory situation of white fat 3 . Plasma-circulating adipokines and pro-inflammatory cytokines that are secreted from the cells with monocyte/macrophage phenotype may represent a mechanism for several obese-related adult health problems like type II diabetes [3][4][5]9 . Along with a clear association between immune-inflammatory responses and obesity, systemic cellular immune modulatory responses other than inflammation in obese targets have been also reported.…”

“…In modern society, obesity is considered a disease that causes incurable adult health problems including type II diabetes, cardiovascular disorders and cancer [1][2][3][4][5] . Recent findings indicate that obesity is a chronic inflammatory disease 3,6,7 .…”

Decreased splenic mRNA expression levels of TNF-α and IL-6 in diet-induced obese animals

“…Different researchers have proposed that obesity is associated with a state of low-degree chronic inflammation (4,13), as indicated by increased plasma concentrations of protein C reactive (PCR), interleukin-6 (IL-6), tumor necrosis factor-~x (TNF-~) and plasminogen activator inhibitor-1 (PAI-1). The inflammatory response seems to affect predominantly adipocytes (15), since they are able to secrete TNF-~x and other inflammatory markers collectively referred to as adipokines (1).…”

Obesity, anemia, and cardiovascular risk in patients with chronic kidney disease: Overview and pathophysiologic insights

“…Additionally, the IL-1 family (IL-1α, IL-1β, and IL-1Ra) has been demonstrated to infl uence fat mass, fat metabolism, and total body mass and has been implicated in inducing insulin resistance [27]. This was thought to be due, in part, to IL-1β's cytotoxicity against islet β cells in non-insulin-dependent DM [28]. IL-1β has been shown to be signifi cantly more elevated in obese insulin-dependent and obese non-insulin-dependent diabetics than nonobese diabetic patients, further suggesting that adipose tissue is a source of the excess IL-1β and thus plays a role in the progression of type 2 DM [28].…”

“…This was thought to be due, in part, to IL-1β's cytotoxicity against islet β cells in non-insulin-dependent DM [28]. IL-1β has been shown to be signifi cantly more elevated in obese insulin-dependent and obese non-insulin-dependent diabetics than nonobese diabetic patients, further suggesting that adipose tissue is a source of the excess IL-1β and thus plays a role in the progression of type 2 DM [28].…”