Fasting Plasma Leptin Level Is a Surrogate Measure of Insulin Sensitivity

Askari, Hasan; Tykodi, Gunjan; Liu, Jianmei; Dagogo‐Jack, Samuel

doi:10.1210/jc.2010-0296

Cited by 48 publications

(31 citation statements)

References 36 publications

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“…Leptin infusion has been shown to ameliorate insulin sensitivity in the skeletal muscle (42), whereas insulin infusion has been shown to increase leptin levels (43), even in physiologic amounts (44). Therefore, it has been suggested that the onset of IR could lead to an increase in leptin secretion as a compensatory response (45), which might explain our findings. Indeed, we observed that insulin sensitivity estimates (fasting insulin, insulin-to-glucose ratio, Matsuda index, AUC insulin , AUC insulin/glucose , and HOMA IR) were moderately and significantly correlated with surrogate markers of inflammation CRP level and leptin, which advocates for a role of inflammation in IR in SLE.…”

mentioning

confidence: 63%

Increased Insulin Resistance and Glucagon Levels in Mild/Inactive Systemic Lupus Erythematosus Patients Despite Normal Glucose Tolerance

Miyake

Gualano

Dantas

et al. 2017

Arthritis Care & Research

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Objective. To assess insulin sensitivity in patients with systemic lupus erythematosus (SLE) in response to a meal tolerance test (MTT). Methods. In this cross-sectional study, 33 adult females with mild/inactive SLE (SLE group) and 16 age-and body mass index-matched female healthy controls (CTRL group) underwent an MTT and were assessed for insulin sensitivity and beta cell function. Skeletal muscle protein expressions of total and membrane insulin-dependent glucose transporter 4 (GLUT-4) were also evaluated (SLE group: n = 10, CTRL group: n = 5); muscle biopsies were performed after MTT. Further measurements included inflammatory cytokines, adipocytokines, physical activity level, body composition, and food intake. Results. SLE and CTRL groups showed similar fasting glucose, glucose response, and skeletal muscle GLUT-4 translocation after MTT. However, the SLE group demonstrated higher fasting insulin levels (P = 0.01; effect size [ES] 1.2), homeostatic model assessment insulin resistance (IR) (P = 0.03; ES 1.1), insulin-to-glucose ratio response to MTT (P = 0.02; ES 1.2), fasting glucagon levels (P = 0.002; ES 2.7), glucagon response to MTT (P = 0.0001; ES 2.6), and a tendency toward lower Matsuda index of whole-body insulin sensitivity (P = 0.06; ES À0.5) when compared with the CTRL group. Fasting proinsulin-to-insulin ratio and proinsulin-to-insulin ratio response to MTT were similar between groups (P > 0.05), while the SLE group showed a higher insulinogenic index when compared with the CTRL group (P = 0.02; ES = 0.9). Conclusion. We have identified that SLE patients had a bi-hormone metabolic abnormality characterized by increased IR and hyperglucagonemia despite normal glucose tolerance and preserved beta cell function and skeletal muscle GLUT-4 translocation. Strategies capable of ameliorating insulin sensitivity to reduce the risk of type 2 diabetes mellitus and cardiovascular disease in SLE may require more than targeting IR alone.

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confidence: 63%

Increased Insulin Resistance and Glucagon Levels in Mild/Inactive Systemic Lupus Erythematosus Patients Despite Normal Glucose Tolerance

Miyake

Gualano

Dantas

et al. 2017

Arthritis Care & Research

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“…32,33 Outside of pregnancy, serum leptin levels are positively correlated with BMI and body fat mass. 34,35 Many studies have investigated the relationship between maternal obesity and circulating leptin levels using plasma or serum samples collected at different gestational ages. 22,23,27,36,37 Although these studies are very heterogeneous and cannot be directly compared, all of them report that overweight women have significantly higher circulating levels of leptin than normal weight women, throughout pregnancy.…”

Section: Leptinmentioning

confidence: 99%

Maternal obesity and inflammatory mediators: A controversial association

Pendeloski

Ono

Torloni

et al. 2017

American J Rep Immunol

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The link between maternal obesity and inflammatory mediators is still unclear. Our aim was to summarize the main findings of recently published studies on this topic. We performed a search in Medline for studies published in the last years on obesity, human pregnancy, and inflammatory mediators. We report the findings of 30 studies.The characteristics and number of participants, study design, gestational age at sample collection, and type of sample varied widely. Approximately two-thirds of them investigated more than one mediator, and 50% included participants in only one trimester of pregnancy. The most frequently investigated mediators were leptin, tumour necrosis factor-alpha (TNF-α), and interleukin (IL)-6. Almost all studies reported an association between maternal obesity, leptin, and C-reactive protein (CRP) serum levels but not with IL-1β and IL-10. The association of IL-6, TNF-α, monocyte chemo-attractant protein-1 (MCP-1), adiponectin, and resistin with maternal obesity is still controversial.To clarify the physiopathological link between maternal obesity and inflammation, more high-quality studies are needed. K E Y W O R D Sadipokine, cytokine, inflammatory mediator, maternal obesity, pregnancy | INTRODUCTIONObesity has more than doubled in the last decades in the general population. Maternal obesity is also increasing. In the United Kingdom, nearly 20% of pregnant women are obese, 1 and in the United States, over 50% of all pregnant women are currently overweight or obese.2 Obesity in pregnancy is associated with both immediate and long term adverse events for both the mother and the offspring, including the risk of metabolic diseases years after delivery.

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“…Adiponectin/leptin ratio may provide a reliable measure of insulin sensitivity [47]. A high carbohydrate diet promotes glucose intolerance and insulin secretion as well as reduces insulin sensitivity, therefore, increases leptin, an insulinresistance surrogate, and reduces adiponectin, an insulin sensitivity surrogate [46,48,49]. A higher consumption of carbohydrate has been found to augment leptin level [44], which is in agreement with the positive association between serum leptin level and energy percent from carbohydrates that has been detected in this study.…”

Section: Discussionmentioning

confidence: 99%

Exploration of micro- and macronutrient consumption and leverage of interaction with adipokines among Jordanian adults

Tayyem¹,

Hijjawi²,

Bawadi³

et al. 2017

clinical-practice

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Methods and Results:A convenient sample of 167 adults was obtained from students and employees in major hospital in Jordan. Serum concentrations of leptin, adiponectin, resistin and interleukine-6 were measured. Nutrients intakes were assessed using a validated quantitative food frequency questionnaire. Higher levels of leptin were associated with the highest consumption of energy from carbohydrate, insoluble, and soluble fiber (P=0.04). Lower levels of leptin were associated with highest consumption of energy from fat (P=0.04), monounsaturated fatty acids (P=0.04) and cholesterol (P=0.02). Lower levels of adiponectin were found among individuals with the highest consumption of carbohydrates (p=0.02) insoluble fibers (P=0.01); and copper (P=0.03). Higher levels of adiponectin were associated with higher consumption of cholesterol (P=0.03). Leptin/adiponectin ratio was positively associated with the intakes of carbohydrates (P=0.04), soluble-(P=0.01) and insoluble fibers (P=0.01) and copper (P=0.03), whereas the ratio was negatively associated with cholesterol (P=0.04), butyric acid (P=0.03) and omega-3 fatty acids (P=0.03). Levels of resistin were only associated with total fiber intake (P=0.04) and levels of interleukine-6 were only associated with cholesterol intake (P=0.01). Conclusion:Our findings suggest that intakes of carbohydrates, fat, cholesterol and fibers are the major dietary factors that may be associated with levels of leptin and adiponectin. Levels of resistin and interleukine-6 may be less associated with diet composition.

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Fasting Plasma Leptin Level Is a Surrogate Measure of Insulin Sensitivity

Abstract: Insulin sensitivity explains about 40% of the variance in fasting leptin levels. Thus, fasting plasma leptin levels probably serve as an endogenous response to ambient insulin resistance and may provide a surrogate measure of insulin action.

Cited by 48 publications

References 36 publications

Increased Insulin Resistance and Glucagon Levels in Mild/Inactive Systemic Lupus Erythematosus Patients Despite Normal Glucose Tolerance

Increased Insulin Resistance and Glucagon Levels in Mild/Inactive Systemic Lupus Erythematosus Patients Despite Normal Glucose Tolerance

Maternal obesity and inflammatory mediators: A controversial association

Exploration of micro- and macronutrient consumption and leverage of interaction with adipokines among Jordanian adults

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