Adiponectin and protection against type 2 diabetes mellitus

Spranger, Joachim; Kroke, Anja; Möhlig, Matthias; Bergmann, Manuela M.; Ristow, Michael; Boeing, Heiner; Pfeiffer, Andreas F. H.

doi:10.1016/s0140-6736(03)12255-6

Cited by 1,020 publications

(716 citation statements)

References 4 publications

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“…A number of previous articles have demonstrated the strong inverse relationship between obesity and adiponectin as well as between diabetes and adiponectin. [34][35][36][37][38] However, in most cases, the diabetic groups had increased BMI, and the effects of obesity vs diabetic status have not been directly addressed. For example, a recent study in 73 type 2 diabetic Japanese subjects demonstrated decreased adiponectin in diabetic subjects.…”

Section: Discussionmentioning

confidence: 99%

Relationships among acylation stimulating protein, adiponectin and complement C3 in lean vs obese type 2 diabetes

et al. 2005

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Objective: The purpose of this study was to determine the relationships between adipocyte hormones acylation stimulating protein (ASP), adiponectin, complement C3 (C3) (ASP precursor) and insulin, C-reactive protein (CRP), lipid profiles and insulin resistance in lean vs obese type 2 diabetes subjects. Subjects: Lean type 2 diabetes subjects (DL n ¼ 27) vs obese type 2 diabetes subjects (DO n ¼ 55) were compared to agematched nondiabetic groups (Obese, OB n ¼ 55 and control, CTL n ¼ 50).Results: The DO group demonstrated significant increases in plasma ASP and C3 with decreases in plasma adiponectin as compared to CTL. Interestingly, these increases in ASP and C3 were as high, or greater, in the DL group in spite of normal weight. By contrast adiponectin in the DL group was comparable to CTL, in spite of marked insulin resistance. C3 correlated with insulin, glucose and homeostasis model assessment of insulin resistance (HOMA-IR); ASP correlated with body mass index (BMI), glucose, insulin and plasma lipid parameters (non-esterified fatty acids (NEFA), triglyceride, cholesterol and apolipoprotein B). Adiponectin correlated with BMI, glucose, NEFA, triglyceride, high-density lipoprotein cholesterol and apolipoprotein A1 but not HOMA-IR, ASP or C3. CRP correlated only with HOMA-IR. Conclusion: Increased ASP and C3 are both associated with diabetes and related lipid factors but are not regulated coordinately. Adiponectin appears to be more closely related to body size (decreased in obese subjects) than insulin resistance in these subjects.

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Section: Discussionmentioning

confidence: 99%

Relationships among acylation stimulating protein, adiponectin and complement C3 in lean vs obese type 2 diabetes

et al. 2005

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“…Naturally, such a mechanism may be involved in vascular dementia that may cause BBB dysfunction, in which APN may play a major role60. Thus, APN could be a dangerous neurodegenerative molecule, and this might explain why little APN is expressed in the nervous system, compared to the strong expression of APN in serum 61. Given the tendency for higher plasma APN in women compared to men,61 we predict that the gender difference regarding the correlation of plasma APN with neuropathology61 may be at least in part attributable to the decrease in BBB integrity in aging, in addition to other mechanisms, including hormonal differences between men and women.…”

Section: Apn May Promote Neurodegeneration In Ad Through Novel Mechanmentioning

confidence: 99%

Importance of adiponectin activity in the pathogenesis of Alzheimer's disease

Waragai

Ho²,

Takamatsu

et al. 2017

Ann Clin Transl Neurol

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A recent study suggested that insulin resistance may play a central role in the pathogenesis of Alzheimer's disease (AD). In this regard, it is of note that upregulation of plasma adiponectin (APN), a benign adipokine that sensitizes the insulin receptor signaling pathway and suppresses inflammation, has recently been associated with the severities of amyloid deposits and cognitive deficits in the elderly, suggesting that APN may enhance the risk of AD. These results are unanticipated because AD has been linked to type II diabetes and other metabolic disorders in which hypoadiponectinemia has been firmly established, and because APN ameliorated neuropathological features in a mouse model of neurodegeneration. Therefore, the objective of this study is to discuss the possible mechanisms underlying the biological actions of APN in the context of AD. Given that insulin receptor signaling is required for normal function of the nervous system, we predict that APN may be upregulated to compensate for compromised activity of the insulin receptor signaling pathway. However, increased APN might be sequestered by tau in the brain, leading to neurotoxic protein aggregation in AD. Alternatively, misfolding of APN may result in downregulation of the insulin/APN signal transduction network, leading to decreased neuroprotective and neurotrophic activities. Thus, it is possible that both ‘gain of function’ and ‘loss of function’ of APN may underlie synaptic dysfunction and neuronal cell death in AD. Such a unique biological mechanism underlying APN function in AD may require a novel therapeutic strategy that is distinct from previous treatment for metabolic disorders.

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“…9,10 An increasing body of evidence has shown low-adiponectin levels to predict risk of developing diabetes. [11][12][13][14][15][16] Although an inverse association has been found between adiponectin and prevalent coronary heart disease (CHD) in crosssectional studies, 17,18 prospective studies have produced conflicting results. [19][20][21][22] It remains uncertain whether adiponectin is a critical factor in the 'common soil' 23 leading to both diabetes and cardiovascular disease.…”

Section: Introductionmentioning

confidence: 99%

Associations of adiponectin with metabolic and vascular risk parameters in the British Regional Heart Study reveal stronger links to insulin resistance-related than to coronory heart disease risk-related parameters

et al. 2007

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Background and aim: Adiponectin is considered by many to be part of the 'common soil' linking type 2 diabetes and coronary heart disease (CHD). We examined the relationship between adiponectin and insulin resistance, metabolic, inflammatory and haemostatic risk factors and hepatic function. Methods and results: The study was carried out in 3640 non-diabetic men aged 60-79 years drawn from general practices in 24 British towns and who were not on warfarin. Adiponectin was associated with waist circumference (inversely), alcohol intake (positively) and physical activity (nonlinearly); no association was seen with cigarette smoking, prevalent CHD or stroke. After adjustment for these factors, adiponectin was significantly inversely associated with insulin resistance, triglyceride, C-reactive protein (but not interleukin 6), tissue plasminogen activator and alanine aminotransferase and positively associated with highdensity lipoprotein cholesterol (HDL-cholesterol) and Factor VIII, factors associated with diabetes. No association was seen with cholesterol, smoking, systolic blood pressure or coagulation factors. Risk of the metabolic syndrome decreased significantly with increasing adiponectin. Conclusion: Adiponectin is inversely associated with factors strongly associated with the development of diabetes. Limited associations with the established major risk factors for CHD suggest adiponectin may be a stronger marker of risk for diabetes than for CHD.

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Adiponectin and protection against type 2 diabetes mellitus

Cited by 1,020 publications

References 4 publications

Relationships among acylation stimulating protein, adiponectin and complement C3 in lean vs obese type 2 diabetes

Relationships among acylation stimulating protein, adiponectin and complement C3 in lean vs obese type 2 diabetes

Importance of adiponectin activity in the pathogenesis of Alzheimer's disease

Associations of adiponectin with metabolic and vascular risk parameters in the British Regional Heart Study reveal stronger links to insulin resistance-related than to coronory heart disease risk-related parameters

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