Role of Metformin for Weight Management in Patients Without Type 2 Diabetes

Desilets, Alicia R; Dhakal-Karki, Sushmita; Dunican, Kaelen C

doi:10.1345/aph.1k656

Cited by 101 publications

(69 citation statements)

References 48 publications

(12 reference statements)

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“…In previous studies, metformin alone has had inconsistent effects on insulin sensitivity with increases from 0 (8) to as much as 30% (13,32,39). Long-term metformin treatment can induce subtle but potentially relevant weight loss (ϳ5-7 kg) that can contribute to enhanced whole body insulin sensitivity (10). Metformin treatment did not cause weight loss in the current study, which may be a reason why there was no independent effect of metformin on insulin Data are means Ϯ SD and are expressed relative to baseline values for each group.…”

Section: Discussionmentioning

confidence: 99%

Combining short-term metformin treatment and one bout of exercise does not increase insulin action in insulin-resistant individuals

Sharoff

Hagobian

Malin

et al. 2010

American Journal of Physiology-Endocrinology and Metabolism

117

133

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Results from the Diabetes Prevention Program highlight the effectiveness of metformin or regular physical activity in the prevention of type 2 diabetes. Independently, metformin and exercise increase insulin sensitivity, but they have not been studied in combination. To assess the combined effects, insulin-resistant subjects ( n = 9) matched for weight, body fat, and aerobic fitness were studied before any treatment (B), after 2–3 wk of 2,000 mg/day metformin (MET), and after metformin plus 40 min of exercise at 65% V̇o2peak (MET + Ex). A second group ( n = 7) was studied at baseline and after an identical bout of exercise with no metformin (Ex). Biopsies of the vastus lateralis were taken at B, after MET, immediately after MET + Ex ( group 1), or immediately after Ex ( group 2). Insulin sensitivity was assessed 4 h postexercise with a euglycemic hyperinsulinemic (40 mU·m2·min−1) clamp enriched with [6,6-2H]glucose. Insulin sensitivity was 54% higher after Ex ( P < 0.01), but there was no change with Met + Ex. Skeletal muscle AMPKα2 activity was elevated threefold ( P < 0.01) after Ex, but there was no increase with MET + Ex. These findings suggest that the combination of short-term metformin treatment and an acute bout of exercise does not enhance insulin sensitivity, and the addition of metformin may attenuate the well-documented effects of exercise alone.

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Section: Discussionmentioning

confidence: 99%

Combining short-term metformin treatment and one bout of exercise does not increase insulin action in insulin-resistant individuals

Sharoff

Hagobian

Malin

et al. 2010

American Journal of Physiology-Endocrinology and Metabolism

117

133

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show abstract

“…Metformin, an oral insulin sensitizer, which improves insulin sensitivity effectively, reduces the incidence of the metabolic syndrome in overweight and obese patients as well helps in losing weight [10]. Long-term follow-up from the Diabetes Prevention Program demonstrated that metformin produced durable weight loss in several ways, with decreased food intake shown to be the primary mechanism [11].…”

Section: Introductionmentioning

confidence: 99%

Protective effects of metformin on reproductive function in obese male rats induced by high-fat diet

Yan

et al. 2015

J Assist Reprod Genet

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Purpose The study aims to elucidate the changes in testicular spermatogenic function in high-fat diet (HFD)-induced obese rats and to evaluate the protective effects of metformin intervention. Methods Male Sprague-Dawley rats (n=18) were randomly divided into a control group (standard diet), an HFD group, and a metformin group (HFD + metformin at 100 mg/kg, once daily by oral gavage). After 8 weeks, rats were euthanized, and the weights of body and testes were measured. Testis and epididymis were dissected and hematoxylin-eosin-stained for histopathological examination and semen parameter analysis. Blood samples were collected for assessment of sex hormones and metabolic parameters (serum glucose, insulin, and leptin). Spermatogenic cell apoptosis was accessed by TUNEL. Results Compared with the control group, the final body weight and weight gain were significantly higher in HFD rats, while the testicle weight and coefficients were lower. In HFD rats, metformin treatment induced weight loss and increased testicle weight (P<0.05). In HFD rats, obvious pathological changes in the testicular tissue were characterized by small, atrophic, and distorted seminiferous tubules and destroyed basement membrane. Metformin treatment protected against the HFD-induced decrease in the number of spermatogonia, Sertoli cells, and Leydig cells (P<0.05); ameliorated the HFD-induced increases in serum glucose, insulin, leptin, and estrogen; and decreased serum testosterone (P<0.05) and reduced the rate of testicular cell apoptosis in obese male rats. Finally, metformin significantly improved semen parameters (including concentration, viability, motility, and normal morphology) in HFD rats (P<0.05). Conclusions HFD-induced obesity in rats results in detrimental effects on spermatogenesis, semen quality, endogenous hormones, and testicular cell apoptosis. Metformin intervention improved the semen parameters, possibly due to its effects on weight loss, increased testicular weight, reduced testicular cell apoptosis, and resulted in restoration of hormonal homeostasis and correction of metabolic disorder.

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“…Metformin also promotes weight loss in the context of polycystic ovary syndrome and has also been employed with some success to prevent weight gain in patients treated with certain antipsychotic agents (Harborne et al 2005;Nieuwenhuis-Ruifrok et al 2009;Praharaj et al 2011). Hence, there is no reason to suspect that weight control benefits of AMPK activation will be confined to diabetics (Desilets et al 2008).…”

Section: Weight Controlmentioning

confidence: 99%

AMPK activation—protean potential for boosting healthspan

McCarty

2013

AGE

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AMP-activated kinase (AMPK) is activated when the cellular (AMP+ADP)/ATP ratio rises; it therefore serves as a detector of cellular "fuel deficiency." AMPK activation is suspected to mediate some of the health-protective effects of long-term calorie restriction. Several drugs and nutraceuticals which slightly and safely impede the efficiency of mitochondrial ATP g e n e r a t i o n -m o s t n o t a b l y m e t f o r m i n a n d berberine-can be employed as clinical AMPK activators and, hence, may have potential as calorie restriction mimetics for extending healthspan. Indeed, current evidence indicates that AMPK activators may reduce risk for atherosclerosis, heart attack, and stroke; help to prevent ventricular hypertrophy and manage congestive failure; ameliorate metabolic syndrome, reduce risk for type 2 diabetes, and aid glycemic control in diabetics; reduce risk for weight gain; decrease risk for a number of common cancers while improving prognosis in cancer therapy; decrease risk for dementia and possibly other neurodegenerative disorders; help to preserve the proper structure of bone and cartilage; and possibly aid in the prevention and control of autoimmunity. While metformin and berberine appear to have the greatest utility as clinical AMPK activators-as reflected by their efficacy in diabetes management-regular ingestion of vinegar, as well as moderate alcohol consumption, may also achieve a modest degree of healthprotective AMPK activation. The activation of AMPK achievable with any of these measures may be potentiated by clinical doses of the drug salicylate, which can bind to AMPK and activate it allosterically.

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Role of Metformin for Weight Management in Patients Without Type 2 Diabetes

Cited by 101 publications

References 48 publications

Combining short-term metformin treatment and one bout of exercise does not increase insulin action in insulin-resistant individuals

Combining short-term metformin treatment and one bout of exercise does not increase insulin action in insulin-resistant individuals

Protective effects of metformin on reproductive function in obese male rats induced by high-fat diet

AMPK activation—protean potential for boosting healthspan

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