Fasting Glucose to Leptin Ratio as a New Diagnostic Marker in Patients with Diabetes Mellitus

Baban, Rayah S.

doi:10.5001/omj.2010.80

Cited by 8 publications

(5 citation statements)

References 22 publications

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“…Additionally, we measured leptin levels since it has been reported by some groups that InsRes is accompanied by leptin resistance, and that the ratio of both hormones can be used as a parameter for measuring metabolic alterations in humans and rodents. 28 We found a significant increase in leptin levels in the HFFD rats as compared with controls (94.5%, Po0.001) as well as a positive correlation bet-ween the two hormones levels (r ¼ 0.6697, P ¼ 0.0280) ( Figure 1C). These data indicate that HFFD-fed rats develop systemic InsRes and elevated levels of leptin, which has also been associated with the development of obesity and InsRes.…”

Section: Short-term High-fat-and-fructose Diet Feeding Induces Obesitmentioning

confidence: 65%

Short-Term High-Fat-and-Fructose Feeding Produces Insulin Signaling Alterations Accompanied by Neurite and Synaptic Reduction and Astroglial Activation in the Rat Hippocampus

Calvo-Ochoa

Hernández‐Ortega

Ferrera

et al. 2014

J Cereb Blood Flow Metab

128

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Chronic consumption of high-fat-and-fructose diets (HFFD) is associated with the development of insulin resistance (InsRes) and obesity. Systemic insulin resistance resulting from long-term HFFD feeding has detrimental consequences on cognitive performance, neurogenesis, and long-term potentiation establishment, accompanied by neuronal alterations in the hippocampus. However, diet-induced hippocampal InsRes has not been reported. Therefore, we investigated whether short-term HFFD feeding produced hippocampal insulin signaling alterations associated with neuronal changes in the hippocampus. Rats were fed with a control diet or an HFFD consisting of 10% lard supplemented chow and 20% high-fructose syrup in the drinking water. Our results show that 7 days of HFFD feeding induce obesity and InsRes, associated with the following alterations in the hippocampus: (1) a decreased insulin signaling; (2) a decreased hippocampal weight; (3) a reduction in dendritic arborization in CA1 and microtubule-associated protein 2 (MAP-2) levels; (4) a decreased dendritic spine number in CA1 and synaptophysin content, along with an increase in tau phosphorylation; and finally, (5) an increase in reactive astrocyte associated with microglial changes. To our knowledge, this is the first report addressing hippocampal insulin signaling, as well as morphologic, structural, and functional modifications due to short-term HFFD feeding in the rat.

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Section: Short-term High-fat-and-fructose Diet Feeding Induces Obesitmentioning

confidence: 65%

Short-Term High-Fat-and-Fructose Feeding Produces Insulin Signaling Alterations Accompanied by Neurite and Synaptic Reduction and Astroglial Activation in the Rat Hippocampus

Calvo-Ochoa

Hernández‐Ortega

Ferrera

et al. 2014

J Cereb Blood Flow Metab

128

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“…This ratio was negatively correlated with SBP, DBP, MAP, and HOMA-IR in men. One study reported that the fasting Glc/I ratio is an appropriate index of insulin sensitivity, but it becomes apparent only when fasting glucose levels are abnormal (39). Similarly, another study reported that it is a weak insulin sensitivity index and is probably similar to 1/insulin in nondiabetic subjects (40).…”

Section: Discussionmentioning

confidence: 99%

Is the combined use of insulin resistance indices, including adipokines, more reliable in metabolic syndrome?

Kural

Erem²,

Yucesan³

2014

Turk J Med Sci

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IntroductionMetabolic syndrome (MetS) is a clustering of cardiovascular risk factors associated with insulin resistance, central adiposity, hyperglycemia, hypertension, hypertriglyceridemia, and low high-density lipoprotein cholesterol (HDL-C) levels (1,2).Adipokines are secreted by adipose tissue and influence a variety of physiological processes such as food intake control, energy homeostasis, insulin sensitivity, angiogenesis, blood pressure regulation, and blood coagulation (3). They play significant roles in the pathogenesis of obesity, MetS, and chronic inflammatory and autoimmune diseases (4). Leptin is one adipokine that contributes to the regulation of body weight, modulation of insulin sensitivity, metabolism, and reproductive function (5). In addition, it affects thermogenesis, hematopoiesis, angiogenesis, and immune homeostasis (6). Another adipokine, adiponectin, produced exclusively by adipocytes of white adipose tissue, plays a significant role in the regulation of insulin sensitivity and has antiatherosclerotic and antiinflammatory properties (3). Resistin is another adipokine that may be involved in sensing the nutritional status-its mRNA level decreases during fasting and increases after food consumption. It is associated with a variety of disorders: obesity, diabetes, atherosclerosis, endothelial dysfunction, thrombosis, angiogenesis, inflammation, and smooth muscle cell dysfunction (4,7). The adipokine visfatin shows insulinlike properties, inhibits glucose release by liver cells, and promotes the storage of triglycerides in preadipocytes (8). It plays roles in immunity, metabolism, aging and Background/aim: To determine the levels of adipokines (leptin, adiponectin, resistin, and visfatin) and the indices of insulin sensitivity/ resistance, and to examine the relationship among them in patients with metabolic syndrome (MetS). Materials and methods:The study groups included 45 subjects with MetS (31 women/14 men), and 45 sex-and age-matched non-MetS healthy volunteers (31 women/14 men). The levels of adipokines were determined by enzyme-linked immunosorbent assay. Results:The levels of leptin and visfatin were significantly higher in the MetS than in the non-MetS subjects (P < 0.01). There was no difference in adiponectin levels in subjects with and without MetS (P = 0.052). Similarly, resistin did not show any statistically significant difference. A statistically significant positive correlation of leptin with insulin levels was observed, while negative correlations of visfatin levels with age, and resistin levels with the ratio of adiponectin to leptin, were found in the MetS (P < 0.05). The combination of adipokines, insulin resistance-sensitivity parameters, and MetS criteria parameters gave more significant differences than a single parameter. Conclusion:Since the parameters mentioned above might affect, interact with, and/or interfere with each other, the combinations of these parameters might give more reliable results to evaluate the insulin resistance/sensitivity in MetS patients.

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“…Migraine sufferers often report cravings for food high in refined sugar and then a migraine develops later [23]. Lower G/I ratio [2,33] and higher I/C ratio [15] depict higher degrees of insulin resistance. In the present study the consumption of sucrose resulted in an immediate decrease in the G/I ratio and increase in I/C ratio in all participants.…”

Section: Migrainementioning

confidence: 98%

Effect of sucrose consumption on serum insulin, serum cortisol and insulin sensitivity in migraine: Evidence of sex differences

Kokavec

2015

Physiology & Behavior

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Fasting Glucose to Leptin Ratio as a New Diagnostic Marker in Patients with Diabetes Mellitus

Abstract: Overall, the glucose/leptin ratio can be used in addition to glucose/insulin ratio, Quantitative Insulin-Sensitivity Check Index, and Homeostasis Model Assessment to accurately assess insulin resistance in subjects with hyperglycemia.

Cited by 8 publications

References 22 publications

Short-Term High-Fat-and-Fructose Feeding Produces Insulin Signaling Alterations Accompanied by Neurite and Synaptic Reduction and Astroglial Activation in the Rat Hippocampus

Short-Term High-Fat-and-Fructose Feeding Produces Insulin Signaling Alterations Accompanied by Neurite and Synaptic Reduction and Astroglial Activation in the Rat Hippocampus

Is the combined use of insulin resistance indices, including adipokines, more reliable in metabolic syndrome?

Effect of sucrose consumption on serum insulin, serum cortisol and insulin sensitivity in migraine: Evidence of sex differences

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