Mathematical model of diabetes and lipid metabolism linked to diet, leptin sensitivity, insulin sensitivity and VLDLTG clearance predicts paths to health and type II diabetes.
Breast cancer patients receiving metformin as treatment for diabetes showed significant reduction in levels of insulin, fasting glucose, CRP, HOMA, leptin, BMI, and Ki-67.
Moreover, CB1 activation is linked to impaired lipid and glucose metabolism and therefore obesity and diabetes, while its antagonism leads to the reduction of plasma triglycerides, low-density lipoprotein cholesterol, leptin, insulin and glucose.
In this cross-sectional study, we measured body mass composition by dual-energy X-ray absorptiometry, wrist circumference, waist-to-height ratio, fasting blood insulin, glucose, lipid profile, adiponectin, and leptin in 280 children with overweight/obesity and without diabetes (age: 7-18 years).
The copy number of mtDNA in various fat stores was higher in obese patients with type 2 diabetes than in obese patients without diabetes or in the control subjects and was related to the levels of leptin and proinflammatory cytokines.
A higher likelihood of asthma remission was associated with a greater decrease in leptin levels, and a higher likelihood of diabetes remission was predicted by a lesser decrease in CC.
HPR was significantly related to duration of diabetes and higher fasting glucose levels (but not consistently with HbA<sub>1c</sub>), and strongly related to all markers of insulin resistance, especially waist circumference, HOMA-IR, QUICKI and leptin.
At the end of the study, in diabetes group, blood glucose level, GLUT2 and galanin expressions increased, while leptin expression decreased when compared to control group.
When examining the correlation network by timing of diabetes onset, there were more perturbations in the network for case subjects diagnosed >10 years versus <5 years after blood collection, with consistent differential correlations of insulin and HbA<sub>1c</sub> C-peptide was the most highly connected node in the early-stage network, whereas leptin was the hub for mid- or late-stage networks.
In contrast, R482 carriers had lower BMI (P < 0.05), leptin (P < 0.01) and fat mass (P < 0.001), but higher intra-/total abdominal fat-mass ratios (P < 0.001) and prevalences of diabetes (P < 0.01) and hypertriglyceridaemia (P < 0.05) than non-R482 carriers, with a trend towards more coronary artery disease.
Antidiabetic activities of CF might be mediated via inhibition of α-amylase and α-glucosidase activities, elevation of serum insulin concentration, and enhancement of insulin and leptin sensitivity in obesity-diabetes rats.
Our results demonstrate that chronic MC4R activation, even in NPY-deficient mice, does not mimic chronic antidiabetic, cardiovascular, or metabolic actions of leptin, and that NPY is not essential for hyperphagia or cardiovascular changes associated with diabetes.
The leptin-resistant db/ db mouse has been extensively studied as a model of diabetes-associated cardiomyopathy; however, data on the functional and morphological alterations in db/ db hearts are conflicting.
Loss of tau also resulted in increased epididymal fat mass and leptin levels, reduced glucose production, and insulin resistance at later ages, leading to complete onset of diabetes.
These results suggest significant associations between BCAA concentrations and those for adiponectin, leptin and HOMA2-IR in individuals without diabetes.
This study assessed short-term memory and biochemical indicators with the levels of ghrelin, leptin, and cortisol between cognitive impairment and normal older adults with or without diabetes.
Selective deletion of LEPR in these neurons with the Cre-loxP system, however, has previously failed to recapitulate, or only marginally recapitulated, the obesity and diabetes that are seen in LEPR-deficient Lepr <sup>db/db</sup> mice, suggesting that AGRP or POMC neurons are not directly required for the effects of leptin in vivo<sup>8-10</sup>.
Multivariable logistic regression analysis showed that leptin (odds ratio [OR] 1.09; 95% confidence interval [CI] 1.04-1.14; p <0.001), diabetes (OR 7.17; CI 1.39-37.00; p = 0.019), body fat mass (OR 1.16; CI 1.02-1.33; p = 0.027); and hemoglobin (OR 2.11; CI 1.15-3.87; p = 0.015) were independently associated with arterial stiffness in HD patients.