Evidence for Insulin Resistance in Nonobese Patients with Polycystic Ovarian Disease

Jialal, Ishwarlal; Naiker, P; Reddi, K.; Moodley, Jagidesa; Joubert, S. M.

doi:10.1210/jcem-64-5-1066

Cited by 93 publications

(47 citation statements)

References 3 publications

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“…Increased skin 5α-reductase activity is thought to be responsible [12]. The relationship of insulin resistance and PCOS is well known [13][14][15][16][17][18]. Overall, about 50-70% of women with PCOS have insulin resistance [19].…”

Section: Discussionmentioning

confidence: 99%

Evaluation of various insulin sensitivity indices in lean idiopathic hirsutism patients

2012

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Hirsutism is characterized by excessive growth of terminal hair in a male pattern. Excessive hair growth in the absence of demonstrable androgen excess in ovulatory women is also referred to as idiopathic hirsutism (IH). IH is diagnosed in women who have hirsutism, normal ovulatory function and normal total or free testosterone levels. IH is a common cause of hirsutism. IH is not associated with any sign of virilization. Its cause is not understood completely. It has been proposed that women with IH have significantly increased cutaneous 5α-reductase activity. The presence or absence of such an association is not clear [1].Polycystic ovary syndrome (PCOS), another cause of hirsutism, is an insulin resistance related syndrome. Abstract. Hirsutism is characterized by excessive growth of terminal hair in a male pattern. Idiopathic hirsutism (IH) is a common cause of hirsutism. Since there are few data demonstrating IH is associated with insulin resistance, we tried to assess various insulin sensitivity indices in lean IH and compare with healthy subjects. A cross-sectional study was performed in 71 lean (BMI between 20-25 kg/m 2 ) women (17-39 years old), 31 with IH and 40 healthy individuals. Blood glucose, insulin, homeostasis model assessment of insulin resistance (HOMA-IR), hepatic insulin sensitivity (ISI HOMA ), Quicky index, reciprocal fasting insulin resistance index, fasting Belfiore index, and fasting glucose/insulin ratio (GIR) were estimated using a single fasting sample of glucose and insulin levels. Raynaud indices calculated using the mathematical estimation in a single fasting sample of insulin levels were determined and compared in two groups. Fasting insulin, Raynaud index, HOMA-IR and Fasting insulin resistance index (FIRI) results were higher in IH group than in controls (p<0.01, for all). Fasting Belfiore index, QUICKI index, ISI HOMA and FIRI -1 results were lower in IH group than in controls (p<0.01, for all). Our study showed that lean IH patients were more insulin resistant than healthy subjects. We propose that insulin sensitivity indices are useful methods for measuring insulin resistance in IH.Key words: Idiopathic hirsutism, Insulin resistance, Lean patients, Insulin sensitivity indices insulin resistance. There are few data demonstrating IH is associated with insulin resistance. Since the pathogenesis of IH is still unclear, we tried to assess various insulin sensitivity indices in lean IH and compare with healthy subjects. materials and methodsA cross-sectional study was performed in 71 lean (BMI between 20-25 kg/m 2 ) women (17-39 years old), 31 with IH and 40 healthy individuals. The protocol was approved by the hospital-based ethics committee. The protocol of the study was explained to all of the subjects. Informed consent was obtained before beginning the study.None of the control subjects had ovarian dysfunction, hirsutism, or hyperandrogenemia. The diagnosis of IH was based on the presence of hirsutism (modified Ferriman-Gallwey score, >8) [2], regular ovulatory menstrual cycles...

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Section: Discussionmentioning

confidence: 99%

Evaluation of various insulin sensitivity indices in lean idiopathic hirsutism patients

2012

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“…Hyperandrogenic women were studied in the follicular phase (days [1][2][3][4][5][6][7][8] of the cycle or after 2 or more months of amenorrhea. Blood samples were obtained before and at 16, 20, and 24 h after 100 tg of nafarelin ([6-D-(2-naphthyl)-alanine]-GnRH acetate; Syntex Research, Palo Alto, CA) was administered as a subcutaneous injection as previously described (20).…”

Section: Experimental Protocolsmentioning

confidence: 99%

“…Women with polycystic ovary syndrome (PCOS)' are at increased risk of developing impaired glucose tolerance (IGT) and non-insulin-dependent diabetes mellitus (NIDDM) (1)(2)(3)(4)(5)(6)(7)(8)(9)(10). 20% of obese women with PCOS develop IGT or frank NIDDM by age 40 yr (3,11), and long-term follow-up of women with polycystic ovaries reveals an increased prevalence of NIDDM compared with controls (9,10).…”

Section: Introductionmentioning

confidence: 99%

“…20% of obese women with PCOS develop IGT or frank NIDDM by age 40 yr (3,11), and long-term follow-up of women with polycystic ovaries reveals an increased prevalence of NIDDM compared with controls (9,10). This increased prevalence of IGT and NIDDM has been ascribed to the insulin resistance characteristic of the syndrome (1)(2)(3)(4)(5)(6)12). Because insulin resistance has been shown to antedate the onset of NIDDM in some studies (13)(14)(15)(16), it has been postulated to be the primary pathogenetic factor in NIDDM.…”

Section: Introductionmentioning

confidence: 99%

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Insulin secretory defects in polycystic ovary syndrome. Relationship to insulin sensitivity and family history of non-insulin-dependent diabetes mellitus.

Ehrmann

Sturis²,

Byrne³

et al. 1995

J. Clin. Invest.

392

181

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The increased prevalence of non-insulin-dependent diabetes mellitus (NIDDM) among women with polycystic ovary syndrome (PCOS) has been ascribed to the insulin resistance characteristic of PCOS. This study was undertaken to determine the role of defects in insulin secretion as well as familial factors to the predisposition to NIDDM seen in PCOS. We studied three groups of women: PCOS with a family history of NIDDM (PCOS FHx POS; n = 11), PCOS without a family history of NIDDM (PCOS FHx NEG; n = 13), and women without PCOS who have a family history of NIDDM (NON-PCOS FHx POS; n = 8). Beta cell function was evaluated during a frequently sampled intravenous glucose tolerance test, by a low dose graded glucose infusion, and by the ability of the beta cell to be entrained by an oscillatory glucose infusion. PCOS FHx POS women were significantly less likely to demonstrate appropriate beta cell compensation for the degree of insulin resistance. The ability of the beta cell to entrain, as judged by the spectral power for insulin secretion rate, was significantly reduced in PCOS FHx POS subjects. In conclusion, a history of NIDDM in a first-degree relative appears to define a subset of PCOS subjects with a greater prevalence of insulin secretory defects. The risk of developing NIDDM imparted by insulin

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“…The significance of this frequently quoted finding was unsure because of the inclusion of control groups in the calculations (Burghen et al, 1980;Chang et al, 1983;Shoupe et aZ., 1983;Jialal et al, 1987). Indeed, when control groups were omitted, no association between insulin and androgen concentrations was found in some groups of women with PCOS (Dunaif et al, 1987;Geffner et al, 1986).…”

Section: Hirsutismmentioning

confidence: 99%

Clinical implications of hyperinsulinaemia in women

Conway¹,

Jacobs²

1993

Clinical Endocrinology

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Evidence for Insulin Resistance in Nonobese Patients with Polycystic Ovarian Disease

Cited by 93 publications

References 3 publications

Evaluation of various insulin sensitivity indices in lean idiopathic hirsutism patients

Evaluation of various insulin sensitivity indices in lean idiopathic hirsutism patients

Insulin secretory defects in polycystic ovary syndrome. Relationship to insulin sensitivity and family history of non-insulin-dependent diabetes mellitus.

Clinical implications of hyperinsulinaemia in women

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