Leptin: An annotated addendum

Remesar, Xavier; Rafecas, I.; López, José Antonio Fernández; Alemany, M

doi:10.1002/(sici)1098-1128(199709)17:5<499::aid-med4>3.0.co;2-p

Cited by 4 publications

(4 citation statements)

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“…If leptin were increasing insulin resistance, then an increase in hyperinsulinemia could be expected and not the reduction in plasma insulin seen in the obese mice in this study. This reduction in plasma insulin is consistent with in vitro studies that have shown an inhibitory effect of leptin on islet insulin secretion (10,17,27,31). The TG content of islets is an important modulator of insulin secretion (19), and leptin has been shown to deplete this (33) and increase the expression of enzymes involved in fatty acid oxidation (40), suggesting a possible mechanism for the reduced hyperinsulinemia in the obese mice.…”

Section: Discussionsupporting

confidence: 84%

Leptin has acute effects on glucose and lipid metabolism in both lean and gold thioglucose-obese mice

Bryson

Phuyal

Swan

et al. 1999

American Journal of Physiology-Endocrinology and Metabolism

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Leptin is reported to have effects in peripheral tissues that are independent of its central effects on food intake and body weight. In this study, the acute effects of a single dose of recombinant mouse leptin on lipid and glucose metabolism in lean and gold thioglucose-injected obese mice were examined. Changes were measured 2 h after leptin injection. In lean mice, liver and white adipose tissue (WAT) lipogenesis was inhibited. The activity of the pyruvate dehydrogenase complex (PDHCa), the rate-determining step for glucose oxidation, was reduced in heart, liver, quadriceps muscle, and both brown and white adipose tissues. Muscle and liver glycogen and liver triglyceride (TG) content was unchanged, but muscle TG was decreased. In obese mice, liver and WAT lipogenesis was inhibited and PDHCa reduced in heart and quadriceps muscle. Muscle and liver glycogen was decreased but not TG. Serum insulin was reduced in obese but not lean mice. These results are consistent with a role for leptin in the maintenance of steady-state energy stores by decreasing lipid synthesis and increasing fat mobilization, with decreased glucose oxidation occurring as a result of increased fatty acid oxidation.

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Section: Discussionsupporting

confidence: 84%

Leptin has acute effects on glucose and lipid metabolism in both lean and gold thioglucose-obese mice

Bryson

Phuyal

Swan

et al. 1999

American Journal of Physiology-Endocrinology and Metabolism

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“…Leptin interacts with other hormones as well. Leptin levels are increased due to high insulin levels, excessive consumption of fat-rich diet, overfeeding, glucocorticoids and their daily rhythms, as well as increased fat tissue in the body (15). On the other hand, fasting, hypoglycemia, cold, cAMP, decreased level of fat tissue in the body all cause a reduction in leptin levels (15).…”

Section: Introductionmentioning

confidence: 99%

Comparative Analysis of Plasma Leptin Levels in Both Genders of Patients with Essential Hypertension and Healthy Subjects

et al. 2004

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While pathogenesis of hypertension is not clearly deciphered yet, increase in body weight, most of the time, is associated with hypertension. There are reports indicating that leptin, product of the Ob gene mainly synthesized in adipocytes, may have role(s) in hypertension, but contribution of the gender is rather contradictive. In the present study, plasma leptin levels in patients of both genders with hypertension and normotensive controls were measured and the relationship between plasma leptin levels and BMI were evaluated in both sexes. Total of 62 patients (31 M/31 F) diagnosed with essential hypertension who were not under any antihypertensive medication were admitted into the study. The control group was composed of 56 (25 M/31 F) age-, BMI- and sex-matched healthy normotensive volunteers. Plasma leptin levels were determined by a commercial ELISA kit. Plasma leptin and leptin/BMI levels (Mean +/- SEM) of women (n:62) were significantly higher than men (n:56) (20.10 +/- 1.47 ng/ml versus 4.72 +/- 0.50 ng/ml; p < 0.0001). Plasma leptin and leptin/BMI levels of patients of both genders with hypertension were significantly higher than in normotensive subjects (p < 0.05). Leptin and leptin/BMI levels in obese hypertensives were higher than obese normotensives (p < 0.05). Obese hypertensive women had higher leptin and leptin/BMI levels than obese normotensive women (p < 0.05). In conclusion, these results support the hypothesis that a possible link exists between leptin and hypertension. Further studies are needed to clarify how increased levels of leptin affects the pathophysiology of hypertension.

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“…However, this possibility apparently conflicts the recent demonstration that fasting down-regulates orexin receptor expression in the rat adrenal glands (Karteris et al, 2005) (see section IV.A.2.). In this connection, we want to recall that leptin, which decreases food intake and body weight (Remesar et al, 1997;Mantzoros and Moschos, 1998;Ahima and Flier, 2000) and interacts with the orexin system at the hypothalamic level (see section V.A. ), displays increased plasma concentrations in obese and hyperglycemic patients with Cushing's syndrome (Leal-Cerro et al, 1996;Blum et al, 1997;Weise et al, 1999).…”

Section: Discussionmentioning

confidence: 99%