Serum bone morphogenetic protein 7, insulin resistance, and insulin secretion in non-diabetic individuals

Zeng, Jun; Jiang, Yao‐Guang; Xiang, Shali; Chen, Bing

doi:10.1016/j.diabres.2011.03.010

Cited by 11 publications

(8 citation statements)

References 14 publications

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“…BMP7 is assumed to promote brown adipocyte differentiation and thermogenesis and thus, influence body weight and energy homeostasis [47], [48]. In lean and obese individuals with normal glucose homeostasis BMP7 correlates with β-cell function, as well as with fasting insulin, but not with anthropometric variables [49]. Noteworthy, BMP7 and DLK1 may be counter-regulated in brown adipocyte differentiation [50].…”

Section: Discussionmentioning

confidence: 99%

Identification of Adipokine Clusters Related to Parameters of Fat Mass, Insulin Sensitivity and Inflammation

et al. 2014

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In obesity, elevated fat mass and ectopic fat accumulation are associated with changes in adipokine secretion, which may link obesity to inflammation and the development of insulin resistance. However, relationships among individual adipokines and between adipokines and parameters of obesity, glucose metabolism or inflammation are largely unknown. Serum concentrations of 20 adipokines were measured in 141 Caucasian obese men (n = 67) and women (n = 74) with a wide range of body weight, glycemia and insulin sensitivity. Unbiased, distance-based hierarchical cluster analyses were performed to recognize patterns among adipokines and their relationship with parameters of obesity, glucose metabolism, insulin sensitivity and inflammation. We identified two major adipokine clusters related to either (1) body fat mass and inflammation (leptin, ANGPTL3, DLL1, chemerin, Nampt, resistin) or insulin sensitivity/hyperglycemia, and lipid metabolism (vaspin, clusterin, glypican 4, progranulin, ANGPTL6, GPX3, RBP4, DLK1, SFRP5, BMP7, adiponectin, CTRP3 and 5, omentin). In addition, we found distinct adipokine clusters in subgroups of patients with or without type 2 diabetes (T2D). Logistic regression analyses revealed ANGPTL6, DLK1, Nampt and progranulin as strongest adipokine correlates of T2D in obese individuals. The panel of 20 adipokines predicted T2D compared to a combination of HbA1c, HOMA-IR and fasting plasma glucose with lower sensitivity (78% versus 91%) and specificity (76% versus 94%). Therefore, adipokine patterns may currently not be clinically useful for the diagnosis of metabolic diseases. Whether adipokine patterns are relevant for the predictive assessment of intervention outcomes needs to be further investigated.

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Section: Discussionmentioning

confidence: 99%

Identification of Adipokine Clusters Related to Parameters of Fat Mass, Insulin Sensitivity and Inflammation

et al. 2014

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“…It should be noted that, in Pparγ ocy −/− mice, the changes in glucose metabolism were attributed mainly to increased insulin sensitivity in fat mass rather than enhanced insulin secretion from the islets, although the capability of BMP7 to induce the conversion of human pancreatic exocrine cells to insulin‐expressing cells has been documented previously . In humans, results from a clinical study in non‐diabetic adults suggested that BMP7 might stimulate insulin secretion and improve β cell function, as indicated by its positive association with the insulin secretion index and fasting insulin, even when insulin resistance, BMI, and age were adjusted, while no association with insulin resistance was observed . Gender and genetic variations in BMP7 in humans may influence its impacts on insulin resistance and diabetes risk …”

Section: The Role Of Osteocyte‐secreted Molecules In Energy Metabolismmentioning

confidence: 97%

“…98 In humans, results from a clinical study in non-diabetic adults suggested that BMP7 might stimulate insulin secretion and improve β cell function, as indicated by its positive association with the insulin secretion index and fasting insulin, even when insulin resistance, BMI, and age were adjusted, while no association with insulin resistance was observed. 99 Gender and genetic variations in BMP7 in humans may influence its impacts on insulin resistance and diabetes risk. 100 Notably, BMP7 has long been reported to improve energy metabolism, mainly by promoting brown adipogenesis 101 and by decreasing food intake.…”

Section: The Role Of Osteocyte-secreted Molecules In Energy Metabolismmentioning

confidence: 99%

Bone: Another potential target to treat, prevent and predict diabetes

Liu¹,

Mosialou

Liu

2018

Diabetes Obesity Metabolism

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Type 2 diabetes mellitus is now a worldwide health problem with increasing prevalence. Mounting efforts have been made to treat, prevent and predict this chronic disease. In recent years, increasing evidence from mice and clinical studies suggests that bone-derived molecules modulate glucose metabolism. This review aims to summarize our current understanding of the interplay between bone and glucose metabolism and to highlight potential new means of therapeutic intervention. The first molecule recognized as a link between bone and glucose metabolism is osteocalcin (OCN), which functions in its active form, that is, undercarboxylated OCN (ucOC). ucOC acts in promoting insulin expression and secretion, facilitating insulin sensitivity, and favouring glucose and fatty acid uptake and utilization. A second bone-derived molecule, lipocalin2, functions in suppressing appetite in mice through its action on the hypothalamus. Osteocytes, the most abundant cells in bone matrix, are suggested to act on the browning of white adipose tissue and energy expenditure through secretion of bone morphogenetic protein 7 and sclerostin. The involvement of bone resorption in glucose homeostasis has also been examined. However, there is evidence indicating the implication of the receptor activator of nuclear factor κ-B ligand, neuropeptide Y, and other known and unidentified bone-derived factors that function in glucose homeostasis. We summarize recent advances and the rationale for treating, preventing and predicting diabetes by skeleton intervention.

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“…white adipose tissue browning enhanced energy expenditure, improved glucose tolerance and insulin sensitivity) and this is mediated by BMP-7; the administration of anti-BMP-7 restored the "worse" phenotype in these mice [5]. Clinical studies showed that BMP-7 was positively associated with insulin secretion and improved β-cell function in non-diabetic patients [73]; this osteokine was found to induce the conversion of human pancreatic exocrine cells to insulin-expressing cells [27]. However, because BMP-7 is expressed by several tissues including bone, kidney and heart, the extent to which bone-derived BMP7 contributes to serum BMP7 and influences energy metabolism needs further exploration [33].…”

Section: Bone Morphogenic Protein (Bmp)-7mentioning

confidence: 98%

Exercise-Dependent Modulation of Bone Metabolism and Bone Endocrine Function: New Findings and Therapeutic Perspectives

Lombardi

2019

J. of SCI. IN SPORT AND EXERCISE

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Physical inactivity is the fourth leading cause of mortality worldwide; regardless of geographic location and income, it is a contributing risk factor to the other three causes. Physical activity is really a drug, a poly-pill; its "regular use" can reduce this risk throughout the activation of a plethora of responses in virtually all the body tissues. The beneficial effects of physical activity on cardiovascular function and hemodynamics are mainly mediated by skeletal muscle, adipose tissue and the immune system via the usage, delivery and distribution of metabolic substrates and improvement in inflammatory status. There is emerging evidence for exercise-dependent changes in bone metabolism as well; with improved bone quality, reduced fracture risk and increased bone endocrine function, the last of which modulates energy metabolism through its effects on pancreatic islet cells, skeletal muscle and adipose tissue. Bone endocrine function relies on the integration of biomechanical stimuli and endocrine signals from other organs and tissues. Here I review current concepts about exercise-dependent modulation of bone endocrine function and its beneficial effects on whole-body metabolism. Several molecular mechanisms have been identified that support this exercise-stimulated bone-mediated metabolic effect and, among these, Wnt signaling, fibroblast growth factor-23, bone morphogenic protein-7, osteocalcin, RANK/RANKL/OPG axis, and lipocalin-2 gave the largest evidences. In conclusion, beside the controversies surrounding technical aspects of the exercise, the efficacy of physical activity in preventing/treating metabolic and inflammatory dysfunctions also passes throughout the bone.

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Serum bone morphogenetic protein 7, insulin resistance, and insulin secretion in non-diabetic individuals

Cited by 11 publications

References 14 publications

Identification of Adipokine Clusters Related to Parameters of Fat Mass, Insulin Sensitivity and Inflammation

Identification of Adipokine Clusters Related to Parameters of Fat Mass, Insulin Sensitivity and Inflammation

Bone: Another potential target to treat, prevent and predict diabetes

Exercise-Dependent Modulation of Bone Metabolism and Bone Endocrine Function: New Findings and Therapeutic Perspectives

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